A bird named Sue

I sometimes wish I was a computer science blogger instead of a life sciences blogger. That would mean, or at least should mean, that I know a lot about computers. Unfortunately I’m not a computer science blogger, and I don’t know anything about computers, and that is why I must apologize for the delay leading to this post. Last Friday my computer died on me, dead as could be. I was working on it, got up for a drink (water, as I’m still free from coffee addiction), and when I got back, my trusty laptop had committed suicide (genetic disposition, no doubt). This event caused considerable grief and made me realize that while I am not addicted to coffee, I sure am addicted to using a computer. That being said, I’m back in ComputerLand, and to make up for the delay I am posting about a really, really cool study.

The research paper for today (published May 2009 in Nature) looks at zebra finches, a type of songbird. The song of zebra finches is like a cultural trait: individual finches have small variations in their song and geographically separated finch groups have local song dialects. Overall, though, the song from the zebra finch in the wild (called the “wildtype song”) can be recognized and described. Songbirds learn to sing during their development by being exposed to adult singing males (females lack a singing ability, but at Zebra Finch Idol, they do the judging). This begs the question: What if baby zebra finches aren’t exposed to singing males? To investigate this question, the group of researchers from New York took zebra finch eggs and raised them individually in sound-proof rooms.

Now a Pop Quiz for my readers, for 20 brownie points:
What happens when baby zebra finches aren’t exposed to adult singing males?

A) They never sing.
B) They sing normally.
C) They sing poorly.
D) They spontaneously break out in “A boy named Sue”.

Think about it: if the song is encoded in their genetic code, then it shouldn’t matter whether they are exposed to it or not, and the answer would be B. If the song isn’t encoded in their genetics and they only learn to sing by imitating adult birds, then the answer would be A. D was a red herring, and the correct answer is actually C. The isolated zebra finches sang, but the sound didn’t really resemble the wildtype song.

Good science is all about asking the right questions. Instead of stopping there and analyzing what went wrong, the researchers thought of a really creative way to address the results. They took a second batch of zebra finch eggs (the second generation), and raised them again individually in a sound proof roof, but this time each baby was raised with one adult bird (a singing tutor) from the first generation (the ones who sang poorly). I’ll spare you the quiz this time: the birds from the second generation learned to sing just like their tutors, poorly. However, their song was slightly different. The rhythm and other characteristics of the second generation song were a little closer to the wildtype song. And so the researchers continued: a third generation of birds was raised, this time with second generation tutors. And believe it or not, each generation sang a little more like the wildtype birds and by generation 4, the song was very similar to the original wildtype song.

The conclusion from the article is that song culture is partly encoded in the genetic profile of a population and partly encoded in the environmental variables. Song culture is also a “multigenerational” phenomenon, because it takes a few generations to emerge. It is a bit disappointing that this study doesn’t also look at the mechanisms of what’s happening. For example, song development is known to be associated with something called neurogenesis, which essentially means the birth of new brain cells. Could it be that over a few generations, there is an orderly progression of connections between the new cells? Are the brain cells and associations between brain cells getting reorganized with each new generation? The researchers do promise to look into it, so I’ll stay tuned and keep you posted.

This is what a zebra finch looks like. Pretty cute, huh?

Reference: De novo establishment of wild-type song culture in the zebra finch. Feher O., Wang H., Saar S., Mitra P.P., Tchernichovski O. Nature 2009 May 3 EPub ahead of print.

To panic or not to panic? An interview with the swine flu.

Due to the current international media hype on the swine flu, I’ve decided to stray from my usual modus operandi (for those of you just tuning in, my modus operandi is to write about a recent and relevant research article (not a news article!) in the life sciences). Instead of a research article, today I cornered the swine flu and grilled him like it was his PhD thesis defense.

Scientific Chick: What kind of name is swine flu?
Swine Flu: It’s a bit funny that I was called swine flu to start with, since I infected humans months before recently taking a liking to pigs in Alberta, Canada. The reason I was called swine flu is because part of my genetic code comes from a flu that usually infects pigs. However, other parts of my genetic sequence come from the avian flu, and some are from the human flu. I guess calling me “human flu” would have been even more panic-inducing. Anyway, I’m not called swine flu anymore, because pork producers thought it would be bad publicity, even though you can’t catch me by eating pork. My new name is the type A H1N1 virus, but I doubt that will stick with the media.

SC: Tell us a little bit about yourself.
SF: Well, I’m a virus. That means I’m tiny (about 100 times smaller than your average bacteria), and I’m essentially a collection of RNA segments (which is similar to DNA) and proteins (my machinery to infect you!) encased in an envelope. My H1N1 name comes from the types of proteins on my surface, hemagglutinin (H) and neuraminidase (N). I can only reproduce (for viruses like me, we say replicate) in living cells. When you catch me, I bind to your cells and weasel my way inside. Once inside your cells, my envelope degrades, and my machinery hijacks yours to start making mini-me’s. Once your cell has made a bunch of new viruses, the cell breaks open and releases all the new viruses so they can go and infect more of your cells. Sneaky, huh?

SC: What makes you special?
SF: Robert Webster, An American flu virologist, recently dubbed me as a “real super-mixed-up virus”. My genetics are so new and confusing that you don’t have any immunity to me. That’s all part of my plan for world domination.

SC: How fast do you spread?
SF: How dare you ask me questions about my reproductive habits? I’m not telling. To find out, you’ll have to analyze my basic reproductive number (R0), which is a variable that describes the number of new infections caused by one infected person.

SC: Will you kill me?
SF: Well, you are annoying me with all your questions, but right now I’d have to say no. It’s still unsure whether I will cause severe disease in many people. According to flu researchers, I apparently don’t seem to be anything different than seasonal flu.

SC: Then why did you kill all those Mexicans?
SF: I thought you’d ask. You should hear all the theories about this! Some think the Mexicans are more susceptible because of basic hygiene and medical care. Others suggest that air pollution aggravates my symptoms. Some think it’s because of genetic predispositions. But virologists think you shouldn’t jump to conclusions like that. The reality is, compared with Mexico, the number of the people I infected in the USA or in a country other than Mexico is still too small to pick up significant mortality rates, so it’s very hard to compare.

SC: Can we prevent you from infecting us?
SF: So far, regular flu-prevention measures apply. Wash your hands, stay away from the coughing sickly-looking person at the office, eat healthy and exercise, and take a deep breath. Should you go out and deplete your local drugstore of its surgical masks stock “just in case”? No, unless you’re a nurse working in the flu ward (and if that’s the case, I’d hope that your masks are provided). Those masks have only been shown to work if infected people wear them (that’s why you see them a lot in Mexico), and are not useful in preventing infection at this stage.

As for vaccines, I happen to know that you’re working hard on developing one. You’re going to have a problem, though. Growing viruses to make vaccines is a slow process, and the world’s influenza vaccine production capacity is limited to about 400 million doses a year. If you want to start making vaccines against me, you’re going to have to sacrifice the making of the regular flu vaccine. A bit of a gamble, isn’t it? Especially considering my seasonal flu brothers are pretty lethal (last year, they killed about half a million people). Good luck figuring that one out.

SC: Can we treat you?
SF: I wish I could say I’m indestructible, but I’m no teenager anymore. I’m treatable with two widely-known and used anti-influenza drugs, oseltamivir (Tamiflu) and zanamivir (Relenza), and countries are stocking up.

SC: You’ve been sequenced. What do you say to that?
SF: You think you’re so smart, and that because you know all the letters in my genetic code, you know everything about me. You fool! You still don’t know how virulent I am, and what my mutation pattern is.

SC: How did you evade our fancy pandemic prevention plans?
SF: I went unnoticed. I was clever and popped up at the end of the regular seasonal flu season, so no one paid attention to me for a while. By the time the World Health Organization and the Center for Disease Control realized what was going on, it was too late to nip me in the bud. Mouahahaha.

SC: Should I panic?
SF: One thing is for sure, it seems like the media wants you to panic. Should you give in to the hysteria? Well, it’s good to keep in mind that so far, I’m just like a regular flu. A friend of mine said it best: it’s good to be aware, but there’s no need to be alarmed.

An excellent graph from a site I like called GraphJam

References
As swine flu circles globe, scientists grapple with basic questions. Cohen J. and Enserink M. Science 2009 324:572-573.
Swine flu goes glocal. Butler D. Nature 2009 458:1082-1083.

The secret to eternal youth? Say goodbye to brownies.

You’ve heard of Atkins. You’re familiar with Weight Watchers. You probably know about the South Beach Diet. Well, there’s a new diet in town, and it’s called the “Longevity Diet”. It’s inspired by a relatively new hot topic in the life sciences called caloric restriction. As the name implies, it essentially means eating less, and it's hailed not so much as a weight loss strategy as an anti-aging solution. While I’m usually excited about new simple ways of changing daily habits to live a healthy life, this one I’m not sold on yet. You may remember that I like cheese. You may also remember that I like brownies. So obviously, I’m not too excited to hear that eating less is extra healthy. Especially since most caloric restrictions studies suggest you have to cut back anywhere from 30% to 60% of what you eat to see an effect.

So far, most of the really convincing data on caloric restriction slowing down the aging process have been carried out in model organisms that fit in your pocket: rats, mice, worms, all the way down to the tiny yeast. I personally would be reluctant to extrapolate those findings to humans. Surely worms don’t have the same kind of relationship with brownies that I do. However, one recent study looks at caloric restriction in healthy humans, and it’s hard not to take notice.

Researchers from Germany took 50 normal-to-overweight elderly subjects (sorry, Mom, in this case, “elderly” means 60ish, but the important thing is to be young at heart!) and divided them into groups. One group was told to not change their eating habits, and one group was put on 30% caloric restriction for 3 months. Before the study and after the 3 months, everyone’s memory was tested using simple tests like remembering a list of words. Well, I’m very sorry to say, but after 3 months, the group who ate less did significantly better at the memory tests. Sad but true.

During the study, the volunteers were monitored for many different biological indicators (such as cholesterol, insulin, inflammation, and cellular stress), in hopes of identifying the mechanisms responsible for the effects of caloric restriction. The one mechanism that really stood out and that showed a solid correlation with the memory improvements is insulin: the group on caloric restriction had lower insulin levels. Insulin is a hormone responsible for taking the sugar out of your blood and storing it in your liver and muscles to use when energy is needed, but it also plays an important role in keeping your brain healthy. When you have less insulin circulating in your body, you become more sensitive to it, and this sharpens and improves how your body (including your brain!) reacts to insulin. This may be why the group who ate less performed better on the memory tests.

So, throw out the cheesecake? I’m going to wait a little before I draw any solid conclusions, as there is still a very ongoing debate over caloric restriction. One side is claiming significant benefits like longevity, healthy aging and protection against age-associated diseases (think Alzheimer’s). The other side is critical of the methods and models used, as well as the contradictory results, and points to the downsides of caloric restriction, especially during the reproductive years. Not eating enough can also lead to the breakdown of muscles (and remember, your heart is a muscle), which is very important to consider if you have an active lifestyle. Interestingly, in this study, the authors show that the caloric restriction group lost a significant amount of weight, but did not lose body fat. Healthy? I think the jury is still out, but hopefully more well-controlled human studies will shed some light on this potentially exciting and easy way to fend off the effects of the ticking clock.

Learn to make these, shorten your healthy life expectancy?

Reference: Caloric restriction improves memory in elderly humans. Witte AV, Fobker M, Gellner R, Knecht S, Flöel A. Proc Natl Acad Sci U S A. 2009 Jan 27;106(4):1255-60.

Your brain's reset key is Zzzz

As a teenager, like many of you I’m sure, I neglected sleep. It seemed that partying all night and then working hard at school all day was the obvious solution to an overbooked schedule. I was rudely awakened a few years later when a good night’s sleep became necessary to merely function the next day (also when I realized what it really meant to have an overbooked schedule). While we know that sleep is essential for survival (at some point, coffee just doesn’t cut it), we know very little about why sleep is so important, and what happens to our brain while we sleep. In a recent issue of Science, a team of researchers made a contribution to this field using sleep-deprived fruit flies.

In the study, researchers looked at synapses, the junctions between brain cells (called neurons). Synapses are important because they relay information from one neuron to the next. Through synaptic connections, neurons form networks, and these networks underlie many complex brain functions like perception and thought.

The researchers cleverly engineered fruit flies to make their synaptic connections fluorescent (for those of you who read my first post, this is an excellent use of GFP). Subsequently, the researchers took images of the flies’ brains, and were able to count the brightly fluorescent synapses. The study first established that flies that hang out with other flies (this is called social enrichment) have more synapses than lonely flies. While this finding is interesting on its own, the researchers didn’t stop there. They took the socially enriched flies and divided them in two groups. The first group of flies was allowed to sleep as much as they wanted for 48 hours while the second group of flies was sleep deprived for 48 hours. Which group of flies do you think had more synapses after the experiment?

Well, the study shows that flies that slept had much fewer synapses than the sleep-deprived ones. Does it surprise you?

Initially, I thought this was a little counter-intuitive. With all this talk about sleep being important for performance and memory, I would have thought that the flies that slept would have had more connections between brain cells. This study suggests exactly the opposite, and shows that sleep acts to downscale the synapses that are created while the flies are awake and experiencing new things. When you think about it, this finding makes sense. If there was no way to “reset” those synapses, we can hypothesize that every time you learn or experience something new, you would get more and more connections between your brain cells. Eventually, we can imagine it would be a complete mess up there, and connections might saturate, leaving no room for anything new. Downscaling your synapses at night while you sleep also helps eliminate the unimportant connections, thereby making the stronger synapses stand out.

So what’s the take-home message? Enough procrastinating on the internet, go to bed!

Reference: Use-dependent plasticity in clock neurons regulates sleep need in Drosophila. Donlea JM, Ramanan N, Shaw PJ. Science. 2009 Apr 3;324(5923):105-8.

How old is compassion?

I recently wrote about natural selection, or the survival of the fittest, in bacteria, which is a pretty ruthless process. When it comes to humans, I’m thankful that we care for the sick and the disabled. Having had a few common health issues myself, I know that in the wild, I probably would not have made it past 15 or 16 years old (ever had mono? I can’t imagine hunting mammoths with mono). That being said, I always assumed that compassion and care for the ill was a relatively new concept, made possible by advances in civilization. A new paleopathology (that’s the study of past diseases) finding suggests compassion may have much earlier roots.

A group of Spanish bone hunters found a very interesting cranium at the Sima de los Huesos site in Spain. The cranium belongs to a child who died between the ages of 5 and 12 years old and who lived at least 530 000 years ago! The cranium has been almost fully reconstructed and clearly shows many signs of malformations. The researchers were able to link those signs to a disease that still exists today called craniosynostosis. This disease can have multiple causes and results in cranial deformities (such as an asymmetrical face) and mental retardation. In this case, the pathology would have been present before birth. So what we have here is that 530 000 years ago, there was a child who was visibly abnormal and affected in a way that he or she probably would not have been able to keep up with the group. The amazing finding of this paper is that this child made it to be at least 5 years old, and probably closer to 10 years old. This suggests not only that the population did not act against the individual who was different or sick during infancy (i.e. they didn’t kill a sick baby, like some other populations have been known to do), but also that they cared for the disabled. Not something I would have expected of our hunter-gatherer ancestors.

An interesting question that springs to mind here is, if humans from the Neanderthal era showed some form of compassion, what about animals? I’ll definitely be keeping my eyes out for more research in this area. This kind of science is my favorite: answer a question, and many more arise (unless we’re talking about my thesis project: in that case, all I want are answers).

As I mentioned, I always thought that caring for the ill was a very recent human behavior, but now I’m not so sure. In any case, I’m just glad to know that our ancestors were not complete jerks.

Image of the cranium from the original article
Gracia A. et al, Craniosynostosis in the Middle Pleistocene human Cranium 14 from the Sima de los Huesos, Atapuerca, Spain. Proc Natl Acad Sci USA, Mar 30 2009.

Sipping booze in the womb makes it taste better during your crazy teenage years

If you’re planning to start a family, or make an addition to your already existing family, you probably know that it’s not a good idea to drink alcohol while you’re pregnant. If you choose to consume alcohol during your pregnancy, Fetal Alcohol Spectrum Disorder, or FASD, may happen to your baby, resulting in a whole range of possible consequences including facial malformations and mental retardation.

There may also be much subtler, lesser-known consequences of prenatal alcohol exposure, such as an increased risk of adolescent alcohol abuse. Two researchers from New-York recently added a piece to this puzzle.

The researchers fed pregnant moms either a diet containing ethanol or a regular diet, and then studied how the offspring reacted towards ethanol once they grew up to be teenagers or adults. Oh, and by pregnant moms I mean pregnant rat moms! The study’s first finding is that the offspring from the ethanol-fed moms enjoyed the taste of ethanol a lot more than the offspring of the regular moms. This was measured using a “lick” test: the teenage rats were given solutions of ethanol in increasing concentrations and the researchers counted how much the rats licked the solution compared with water. To try to better understand this finding, the researchers then did the same test but for a bitter tasting liquid. They found that teenage rats exposed to prenatal ethanol had a much better tolerance for the taste of the bitter liquid. Since rats are known to think that alcohol tastes both bitter and sweet, the researchers then tested whether the teenage rats from ethanol-fed moms also thought sugar tasted sweeter than the other rats, but there was no difference there. So this means that the rats that were exposed to ethanol in the womb find that ethanol tastes less bitter and equally sweet as regular rats, tipping the balance towards tasty and away from aversive.

The rats were then tested on how they perceived the smell of ethanol. Sure enough, the teenage rats from ethanol-fed moms seemed to appreciate the smell of ethanol more than the normal rats. Furthermore, their appreciation of the smell also led them to consume more ethanol!

Taken together, this means that exposing rats to ethanol in the womb would lead them to drink more as teenagers by making ethanol taste and smell better. The good news is these findings do not persist into adulthood. Even then, this study puts forward very relevant findings, especially since ethanol exposure during gestation is the best predictor of teenage abuse. The research offers a simple explanation: FASD teenagers may consume more alcohol simple because to them, beer tastes like triple-chocolate brownie fudge sundae with cookie dough to them (that’s the most delicious-sounding analogy I could come up with!). The researchers also point out that other drugs such as tobacco or marijuana have similar chemical smell and taste signatures, and therefore these findings may have broad implications for the link between maternal drug use and how vulnerable you are as a child or teenager.

Personally, the enjoyment I derive from alcohol consumption doesn’t nearly outweigh the consequences of potentially booze crazy teenagers. When the time comes to grow a family, I won’t be taking any chances, thank you very much.

Like music to my brain

According to a new study, you don’t need to be a psychic mind reader to connect with someone else through your brain. All you need is a little jazz.

In everyday life, we often have to coordinate our actions with others. Playing team sports, playing music instruments or singing in a group, dancing, even walking with someone side by side all require that we pay attention to what other people are doing and coordinate together (of course, if I’m dancing, I am generally unable to pay attention to anything but myself, so don’t bank on it). What’s more, coordinating with other people doesn’t only happen when we’re moving. Bonding socially, like when you really hit if off with your speed date and you gaze lovingly in each other’s eyes, also requires coordinated activity.

So what allows us to connect with other people’s minds to sync up with them while dancing or dating? Well, the mechanism for coordinating activities needs to meet two constraints. First, it has to be fast. If you’re trying to dance with me, you only have a split second to react before I stomp your toes mercilessly. Second, it needs to integrate sensory information (where is my foot?), motor activity (removing foot from stomping zone) and brain activity. The best candidate to meet these constraints may be brain oscillations. The cells in your brain (neurons) communicate through electrical signals, and these can be measured using a technique called electroencephalography (EEG). The oscillations are fast, and they bind information in your brain that is related, but not necessarily in the same area. On top of that, we know that these brain oscillations are involved in perception and motor activity. A team of researchers from Germany and Austria set out to examine what happens to those brain waves when we coordinate with others.

In the study, the researchers investigate if two guitarists playing jazz together will have synchronized brain waves. They measure EEG frequency and synchrony during the preparatory period (when the two guitarists are getting ready to start and are listening to a metronome giving them the beat), when they start playing the piece, later during the piece, and after the piece. And, because I’m sure you’re dying to know, the music they played was a jazz-fusion piece composed by Alexander Buck.

The results show that the brains of the guitarists exhibit synchronized brain waves during the preparatory period, at play onset, during the piece, but not at the end when the show is over. The highest level of synchronization is at the moment just when they start playing together.

There are a few limitations to this study. The sample size is small, only 8 pairs of guitarists (though all of them showed synchronization). The other limitation is that both guitarists in a given pair get the same sensory information (they hear the same metronome, are in the same room, etc) and they make the same motor movements (as they are playing the same piece), so it could just be that their brains react in a similar way. But, given the timing and the frequencies of the brain wave synchronization, the authors make a good case for this synchronization resulting from interactions between the two guitarists and not just similarities in the sensory input and motor output.

That our brain waves sync up with others is a pretty neat finding and could explain our ability to coordinate with others when we are engaging in many different activities. This may also have implications for interpersonal relations, such as mother and child bonding. To dig a bit deeper, I wish the researchers had done the same experiment on two people playing Guitar Hero. Would the brain waves synchronize if the guitarists are paying attention to a cue from the screen instead of each other? What do you think? What implications does this finding have for our increasingly virtual modes of communication and interaction?

A person wearing electrodes for EEG