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Tag: Science

Science of Social Networks

Another month has gone by which means another paper to cover!

image This month, instead of covering my usual stomping grounds of biology or chemistry, I decided to look into something a little bit more related to my work in venture capital: social networks!

The power behind the social network concept goes beyond just the number of users. Facebook’s 500 million users is pretty damn compelling, but what brings it home is that by focusing on relationships between people rather than the people themselves, social networks turn into a very interesting channel for information consumption and influence.

This month’s paper (from Damon Centola at MIT Sloan) covered influence – specifically, how different social network structures (or “topologies” if you want to be snooty and academic about it) might have different influences on the people in the networks. More specifically, it asked the question of what social network would you expect to be better able to influence behavior: one which is more “viral”, in the sense that connections aren’t clustered (i.e., I’m as likely to be friends with my friend’s friends as people my friends don’t know), or one which is more “clustered” (i.e., my friends are likely to be friends with one another).

It’s an interesting question, and I found this paper notable for two reasons. First, its the most rigorous social networking experiment I’ve ever seen. Granted, this isn’t saying very much. Most social network/graph studies are observational, but I was impressed by the methodology and the attempt to strip out as much bias and extraneous factors as possible:

  • The behavior being tested was whether or not they would sign up and re-visit a particular health forum. This forum had to be valuable enough to get people to use it (and actually contribute to it), but also unknown and inaccessible to the rest of the world (as to avoid additional social cues from the user’s “real world” social network).
  • The author (and I do mean one single author: pretty rare these days for a Science paper as far as I know) created different social graphs which were superficially identical (same number of users, same number of contacts per user) but had the different network structures he wanted to test(one structure had subgroups of tightly inter-connected users, the other structure had random connections scattered across the network). The figure below shows one example of the network structures: the black lines show connections between people. On the left-hand-side is the highly clustered social graph – the individual users are only connected to people “next to them”. The right-hand-side is the more “viral” social graph, where users can be connected to any user across the social network.
  • The users made profiles (with user name, avatar, and stated health interests), but to preserve anonymity (and limit the impact of a person’s “real world” social network on a user), the user names were blinded and users were not allowed to directly communicate (except in an anonymized fashion through the health forum) or add/remove contacts
  • However, whenever a user’s contacts participated in the health forum, the user would be notified.

The result was a somewhat bizarre and artificial “network” – but its certainly a very creative (and probably as good as it can get) means of turning social networking studies into a rigorous study with real controlled experiments.

Second, the conclusion is interesting and has many implications for people who want to use social networks to influence people. Virality may be a remarkably fast way to get people to hear about something, but the paper concludes that virality does not necessarily translate into people acting. The author conducted 6 different trials with slightly different network topologies (number of users ranged from 98 to 144, number of contacts per user ranged from 6 to 8). The results are in the graph below which shows the fraction of the users who joined the forum over time. As you can see, the clustered networks (solid circles) had much higher and faster adoption than the “viral” networks (open triangles):


Why would this be? The author’s standing theory is that while “viral” networks might be faster at disseminating information (e.g., a funny video), clustered networks work better at driving behavior because you get more reinforcement from your friends. In a clustered network, if you have one friend join the forum, chances are the two of you will have a mutual friend who will also join. At a very basic level, this means you get the same cue to join the forum from two of your friends. In a un-clustered network, however, if you have one friend join the forum, the two of you are less likely to have a mutual friend, and so you are less likely to receive that second cue.

Does this matter? According to the study, someone who had two contacts join the forum was ~75% more likely to join than someone who only had one contact join. And, someone who had four contacts join was ~150% more likely to join than someone who only had one contact. While this effect rapidly diminshes with more contacts (having five or six contacts join made relatively little difference compared with four), its a powerful illustration of quality vs. speed in a social network – something which is also borne out by the fact that while only 15% of people who only had one contact join returned to the forum, 35-45% of users who had multiple contacts join did.

This was definitely a very impressive and well-designed study. While it would be fair to attack the study for its artificiality, I don’t really think there’s any other way to systematically strip out the  biases that are intrinsic to most observational (not a controlled experiment) studies of social networks.

Where I do think this was lacking (and maybe the researcher has already teed this up) is the black-and-white nature of the study. What I mean by this is while I find the argument that network clustering helps drive greater behavior plausible, I think there needs to be a more rigorous/mathematical conception – how “clustered” does a network need to be? If a network is overly clustered, then it loses the virality which helps to spread ideas more quickly and widely – is there an optimal balance somewhere in the middle? Also, the paper only dug, on a very superficial level, into how network size and the number of contacts per user might impact this. I think further experimental and mathematical modeling/computational studies would be nice to really flesh this out.

Paper: Centola, Damon. “The Spread of Behavior in an Online Social Network Experiment.” Science 329 (Sep 2010) – doi:10.1126/science.1185231

(Image credit – social network diagram) (Figures 1 and 2 from paper)


How You Might Cure Asian Glow

image The paper I read for the past month is something that is very near and dear to my heart. As is commonly known, individuals of Asian ancestry are more likely to experience dizziness and flushed skin after drinking alcohol. This is due to the prevalence of a genetic defect in the Asian population which affects an enzyme called Aldehyde Dehydrogenase 2 (ALDH2). ALDH2 processes one of the by-products of alcohol consumption (acetaldehyde). In people with the genetic defect, ALDH2 works very poorly. So, people with the ALDH2 defect build up higher levels of acetaldehyde which leads them to get drunker (and thus hung-over/sick/etc) quicker. This is a problem for someone like me, who needs to drink a (comically) large amount of water to be able to socialize properly while drinking wine/beer/liquor. Interestingly, the anti-drinking drug Disulfiram (sold as “Antabuse” and “Antabus”) helps alcoholics keep off of alcohol by basically shutting down a person’s ALDH2, effectively giving them “Asian alcohol-induced flushing syndrome” (aka an Asian person’s inability to hold their liquor) and making them get drunk and sick very quickly.


So, what can you do? At this point, nothing really (except, either avoid alcohol or drink a ton of water when you do drink). But, I look forward to the day when there may actually be a solution. A group at Stanford recently identified a small molecule, Alda-1 (chemical structure above), which not only increases the effectiveness of normal ALDH2, but can help “rescue” defective ALDH2!

Have we found the molecule which I have been searching for ever since I started drinking? Jury’s still out, but the same group at Stanford partnered with structural biologists at Indiana University to conduct some experiments on Alda-1 to try to find out how it works.

To do this, and why this paper was published in Nature Structural and Molecular Biology rather than another journal, they used a technique called X-ray Crystallography to “see” if (and how) Alda-1 interacts with ALDH2. Some of the results of these experiments are shown on the left. The top (panel b) shows a 3D structure of the “defective’ version of ALDH2. If you’re new to structural biology papers, this will take some time getting used to it, but if you look carefully, you can see that ALDH2 is a tetramer: there are 4 identical pieces (in the top-left, top-right, bottom-left, bottom-right) which are attached together in the middle.

It’s not clear from this picture, but the defective version of the enzyme differs from the normal because it is unable to maintain the 3D structure needed to link up with a coenzyme (a chemical needed by enzymes which do this sort of chemical reaction to be able to work properly) called NAD+ or even carry out the reaction (the “active site”, or the part of the enzyme which actually carries out the reaction, is “disrupted” in the mutant).

So what does Alda-1 do, then? In the bottom (panel c), you can see where the Alda-1 molecules (colored in yellow) are when they interact with ALDH2.  While the yellow molecules have a number of impacts on ALHD2’s 3D structure, the most obvious changes are highlighted in pink (those have no clear counterpart in panel b). This is the secret of Alda-1: it actually changes the shape of ALDH2, (partially) restoring the enzyme’s ability to bind with NAD+ and carry out the chemical reactions needed to process acetaldehyde, and all without actually directly touching the active site (this is something which you can’t see in the panel I shared above, but you can make out from other X-ray crystallography models in the paper).

The result? If you look at the chart below, you’ll see two relationships at play. First, the greater the amount of co-enzyme NAD+ (on the horizontal axis), the faster the reaction speed (on the vertical axis). But, if you increase the amount of Alda-1 from 0 uM (the bottom-most curve) to 30 uM (the highest-most curve), you see a dramatic increase in the enzyme’s reaction speed, for the same amount of NAD+. So, does Alda-1 activate ALDH2? Judging from this chart, it definitely does.

Alda-1 is particularly interesting because most of the chemicals/drugs which we are able to develop work by breaking, de-activating, or inhibiting something. Have a cold? Break the chemical pathways which lead to runny noses. Suffering from depression? De-activate the process which cleans up serotonin (“happiness” chemicals in the brain) quickly. After all, its much easier to break something than it is to fix/create something. But, instead, Alda-1 is actually an activator (rather than a de-activator), which the authors of the study leave as a tantalizing opportunity for medical science:

This work suggests that it may be possible to rationally design similar molecular chaperones for other mutant enzymes by exploiting the binding of compounds to sites adjacent to the structurally disrupted regions, thus avoiding the possibility of enzymatic inhibition entirely independent of the conditions in which the enzyme operates.

If only it were that easy (it’s not)…

Where should we go from here? Frankly, while the paper tackled a very interesting topic in a pretty rigorous fashion, I felt that a lot of the conclusions being drawn were not clear from the presented experimental results (which is why this post is a bit on the vague side on some of those details).

I certainly understand the difficulty when the study is on phenomena which is molecular in nature (does the enzyme work? are the amino acids in the right location?). But, I personally felt a significant part of the paper was more conjecture than evidence, and while I’m sure the folks making the hypotheses are very experienced, I would like to see more experimental data to back up their theories. A well-designed set of site-directed mutagenesis (mutating specific parts of ALDH2 in the lab to play around with they hypotheses that the group put out) and well-tailored experiments and rounds of X-ray crystallography could help shed a little more light on their fascinating idea.

Paper: Perez-Miller et al. “Alda-1 is an agonist and chemical chaperone for the common human aldehyde dehydrogenase 2 variant.” Nature Structural and Molecular Biology 17:2 (Feb 2010) –doi:10.1038/nsmb.1737

(Image credit) (Image credit) (figures from Figure 4 from paper)


Diet Coke + Mentos = Paper

Unless you just discovered YouTube yesterday, you’ve probably seen countless videos of (and maybe even have tried?) the infamous Diet Coke + Mentos reaction… which brings us to the subject of this month’s (belated) paper that I will blog about.

An enterprising physics professor from Appalachian State University decided to have her sophomore physics class take a fairly rigorous look at what drives the Diet Coke + Mentos reaction and what factors might influence its strength and speed. They were not only able to publish their results in the American Journal of Physics, but the students were also given an opportunity to present their findings in a poster session (Professor Coffey reflected on the experience in a presentation she gave). In my humble opinion, this is science education at its finest: instead of having students re-hash boring experiments which they already know the results of, this allowed them to do fairly original research in a field which they probably had more interest in than in the typical science lab course.

So, what did they find?

The first thing they found is that it’s not an acid-base reaction. A lot of people, myself included, believe the diet coke + Mentos reaction is the same as the baking soda + vinegar “volcano” reactions that we all did as kids. Apparently, we were dead wrong, as the paper points out:

The pH of the diet Coke prior to the reaction was 3.0, and the pH of the diet Coke after the mint Mentos reaction was also 3.0. The lack of change in the pH supports the conclusion that the Mint Mentos–Diet Coke reaction is not an acid-base reaction. This conclusion is also supported by the ingredients in the Mentos, none of which are basic: sugar, glucose, syrup, hydrogenated coconut oil, gelatin, dextrin, natural flavor, corn starch, and gum arabic … An impressive acid-base reaction can be generated by adding baking soda to Diet Coke. The pH of the Diet Coke after the baking soda reaction was 6.1, indicating that much of the acid present in the Diet Coke was neutralized by the reaction.

Secondly, the “reaction” is not chemical (no new compounds are created), but a physical response because the Mentos makes bubbles easier to form. The Mentos triggers bubble formation because the surface of the Mentos is itself extremely rough which allows bubbles to aggregate (like how adding string/popsicle stick to an oversaturated mixture of sugar and water is used to make rock candy). But that doesn’t explain why the Mentos + Diet Coke reaction works so well. The logic blew my mind but, in retrospect, is pretty simple. Certain liquids are more “bubbly” by nature – think soapy water vs. regular water. Why? Because the energy that’s needed to form a bubble is lower than the energy available from the environment (e.g., thermal energy). So, the question is, what makes a liquid more “bubbly”? One way is to heat the liquid (heating up Coke makes it more bubbly because heating the carbon dioxide inside the soda gives the gas more thermal energy to draw upon), which the students were able to confirm when they looked at how much mass was lost during a Mentos + Diet coke reaction under three different temperatures (Table 3 below):

What else? It turns out that what other chemicals a liquid has dissolved is capable of changing the ease at which bubbles are made. Physicists/chemists will recognize this “ease” as surface tension (how tightly the surface of a liquid pulls on itself) which you can see visually as a change in the contact angle (the angle that the bubble forms against a flat surface, see below):

The larger the angle, the stronger the surface tension (the more tightly the liquid tries to pull in on itself to become a sphere). So, what happens when we add the artificial sweetener aspartame and potassium benzoate (both ingredients in Diet Coke) to water? As you can see in Figure 4 below, the contact angle in (b) [aspartame] and (c) [potassium benzoate] are smaller than (a) [pure water]. Translation: if you add aspartame and/or potassium benzoate to water, you reduce the amount of work that needs to be done by the solution to create a bubble. Table 4 below that shows the contact angles of a variety of solutions that the students tested as well as the amount of work needed to create a bubble relative to pure water:

This table also shows why you use Diet Coke rather than regular Coke (basically sugar-water) to do the Mentos thing – regular coke has a higher contact angle (and ~20% more energy needed to make a bubble).

Another factor which the paper considers is how long it takes the dropped Mentos to sink to the bottom. The faster a Mentos falls to the bottom, the longer the “average distance” that a bubble needs to travel to get to the surface. As bubbles themselves attract more bubbles, this means that the Mentos which fall to the bottom the fastest will have the strongest explosions. As the paper points out:

The speed with which the sample falls through the liquid is also a major factor. We used a video camera to measure the time it took for Mentos, rock salt, Wint-o-Green Lifesavers, and playground sand to fall through water from the top of the water line to the bottom of a clear 2 l bottle. The average times were 0.7 s for the Mentos, 1.0 s for the rock salt and the Lifesavers, and 1.5 s for the sand … If the growth of carbon  dioxide bubbles on the sample takes place at the bottom of the bottle, then the bubbles formed will detach from the sample and rise up the bottle. The bubbles then act as growth sites, where the carbon dioxide still dissolved in the solution moves into the rising bubbles, causing even more liberation of carbon dioxide from the bottle. If the bubbles must travel farther through the liquid, the reaction will be more explosive.

So, in conclusion, what makes a Diet Coke + Mentos reaction stronger?

  • Temperature (hotter = stronger)
  • Adding substances which reduce the surface tension/contact angle
  • Increasing the speed at which the Mentos sink to the bottom (faster = stronger)

I wish I had done something like this when I was in college! The paper itself also goes into a lot of other things, like the use of an atomic force microscope and scanning electron microscopes to measure the “roughness” of the surface of the Mentos, so if you’re interested in additional things which can affect the strength of the reaction (or if you’re a science teacher interested in coming up with a cool project for your students), I’d strongly encourage taking a look at the paper!

Paper: Coffey, T. “Diet Coke and Mentos: What is really behind this physical reaction?”. American Journal of Physics 76:6 (Jun 2008) – doi: 10.1119/1.2888546

(Table 3, Figure 4, Table 5 from paper) (Contact angle description from presentation)


Life without Oxygen

No, that’s not a reference to a Jordin Sparks/Chris Brown song, its the theme for the paper of the month.

imageThis month, in expression of my gratitude to the kind folks at Open Access publisher BioMedCentral for sending me a “clone” of their very adorable mascot Gulliver (picture left), I have decided to do a post spotlighting a very interesting BMC Biology paper on the discovery of metazoans (creatures in the Animal Kingdom) which live in environments completely devoid of oxygen.

The researchers began their quest by looking at the L’Atalante basin (see below), a so-called deep hypersaline anoxic basin (DHAB) in the Mediterranean Sea. The area in question is over 3 km deep, and is rich in hydrogen sulfide and nearly saturated with salt, the result of which prevents oxygen from less salty waters from mixing into the anoxic (without oxygen) zone.


Now, scientists have known about single-celled bacteria and protozoans capable of living without oxygen for quite some time – and so they were expecting to find tons of those in the anoxic sediments in L’Atalante. What they were hoping to find, however, were multicellular animals capable of living permanently there as well. And find them they did. The researchers, in sifting through the sediment, were able to find three species of living, microscopic (~1 millimeter in size, see below) Loriciferans (themselves a newly discovered, but highly diverse set of creatures).


After verifying that they were alive (and not just dead Loriciferans who sank from another layer of water) and able to do basic things like metabolism without air (and not just air-breathers who were “visiting” the anoxic sediments), the researchers set out to try to determine how these Loriciferans were able to survive:

  • without oxygen
  • in such a toxic environment (Hydrogen Sulfides are strong reducing agents)
  • in an environment as salty as the DHAB

Although the researchers didn’t answer these questions with the level of rigor I would have liked to see, they did make two interesting observations which suggest the sorts of adaptations these creatures evolved to cope:

  • Chemical composition of their bodies: The researchers were able to show (see table below) that Loriciferans from the L’Atalante DHAB had higher levels of Magnesium, Silicon, Iron, and Bromine then their non-anoxic cousins, but lower levels of Calcium, Copper, and Zinc. While this wasn’t completely explained, one might hazard a guess that to survive the harsh environment, these Loriciferans evolved new body structure which used different elements to help cope with/shield themselves from the harsh exterior.
  • No mitochondria, only hydrogenosomes: Almost all oxygen-breathing cells have little organelles in them called mitochondria. Mitochondria are responsible for using oxygen to help convert metabolic products into energy cells can consume. When the researchers applied an electron microscope to the cells of these oxygen-free Loriciferans, they were unable to find any mitochondria. Instead, they found an abundance of hydrogenosome-like structures (below, see all the “H”’s). Hydrogenosomes have previously been found in single-celled creatures which live without oxygen. They use hydrogen, instead of oxygen, to help a cell get energy. This is the first time hydrogenosome-like structures have been found in a multi-cellular creature and probably are a vital adaptation for the Loriciferans in order to let them survive in the DHABs.

Found 3 new species of animal life capable of surviving without oxygen? Sounds like a naturalist’s dream come true. But where does one go from here? From my perspective, I’m most interested in two things.

The first is an extension of the studies the researchers conducted on how these creatures have been able to survive. Identifying “hydrogenosome-like organelles” and high-level “chemical/structural adaptations” is cool, but unsatisfying for anyone trained in basic biology. I want to understand how similar those hydrogenosome-like structures are to hydrogenosomes from single-celled creatures. I want to know what genes are responsible for the hydrogenosome-like structures. I want to understand what the different chemical and structural adaptations do!

The second area of investigation is ecological in nature. What exactly does the food web look like down there? Its great that we’ve found single-celled and multi-cellular creatures, but how do they interact?

Paper: Danovaro, Roberto et al. “The first metazoa living in permanently anoxic conditions.” BMC Biology 8:30 (6 Apr 2010) – doi:10.1186/1741-7007-8-30

(Image credit – Gulliver’s Facebook page) (Figures from Additional File 1, Figure 1, Additional File 4, Figure 4 of paper)

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Reading for value

My buddy Bill shared an article on Google Reader about the demise of Newsweek which linked to this New York Times article (does anyone else find it ironic that one newspaper experiencing financial problems is calling out another publication’s financial problems?):

American newsweeklies were built on original reporting of Large Events, helping readers make sense of a complicated world, but it is a costly endeavor with diminishing returns during an era of commodified and chewed-over news. Both The Economist and The Week were built, rather Web-like, to “borrow” the reporting and then spread analysis on top, thereby making a sundae without having to crank the ice cream maker.

And in this instance, the foreignness of the brands gives the reader an intellectual sheen that once Olympian domestic brands can’t. The Economist and The Week not only make you smarter at cocktail parties by giving you a brief on the week events, but name-checking them will make you sound in the know. Mention Newsweek and people will wonder whether you’ve been going to the dentist a lot lately.

Don’t you love British wit? 🙂

I’m an avid reader of The Economist, and Bill’s shared article got me thinking of why it is that I read The Economist (and many of the other things in my reading list) rather than the numerous other publications out there:

  1. It makes me look smarter. Okay, lets cover the least important (albeit still true) reason first, so I can get it out of the way and focus on the more substantive stuff :-).
  2. It’s analytical. I’m an analytical guy. If there’s one thing consulting has taught me, its that a reasoned conclusion requires both quantitative and qualitative analysis. I’m not satisfied with soundbytes, and I’m not satisfied with superficial reasoning. But, I probably don’t have the time to follow each thread/claim to its origin, nor do I have the time to crunch through all the numbers. Enter The Economist. How many other publications do you know who’ve created an index for measuring purchasing-power parity based on McDonald’s Big Mac? Or run their own quantitative models on the Greek economy to project how the Greek debt situation might look 5 years from now? Or are even in the business of selling macroeconomic analytical data?
  3. It’s opinionated, but still balanced and rigorous. A lot of newspapers strive to be “unbiased.” I think that’s the wrong approach. There are few articles in The Economist which I would say are truly unbiased. And much to its benefit, I might add. When done correctly, having an opinion means doing the necessary research and analysis and thinking. It means carefully considering opposing views. What distinguishes The Economist’s approach is, even if I disagree with the opinion they conclude with, I am given plenty of the background needed to disagree. What newspapers should focus on is not to provide “unbiased” coverage, but balanced (as in carefully presenting all sides of an issue) and rigorous (going beneath the soundbytes).
  4. It’s timely enough. As a weekly, The Economist can’t exactly provide the up-to-the-minute coverage that cable news networks provide (although a lot of that can be remedied if you just check their website). But, frankly, unless you’re a day-trader or a diplomat, I fail to see why you would ever need to know everything on a “as-it-happens” basis. And, if the tradeoff for not getting the news “as-it-happens” is missing out on hours of repeated soundbytes and the very trite cable news network commentary, then I am more than happy to make that tradeoff.
  5. Original content/coverage. Related to the previous point, although it may not be as timely as a cable news network, the Economist also goes places most cable news networks don’t go. It’s the one place I know I can go to get decent analysis of happenings in the Middle East, Africa, Latin America, Eastern Europe, and Southeast Asia – parts of the world that the cable news networks and major newspapers ignore in favor of endlessly hyping up soundbyte-ridden coverage of more “popular” news items. Also unlike many news sources, they’re also one of the few I can reliably turn to who provide decent science coverage in a way which is respectful of scientists and what they actually found rather than what the newspaper thinks the public is interested in the scientists finding.
  6. It’s witty/doesn’t take itself too seriously. Let’s forget, just for a moment, the witty phrasings/titles that are all over The Economist. Take a look at these covers, and tell me that this is a magazine that takes itself too seriously:

image image image

The interesting thing is, without even thinking about it, the list of news-y blogs/web feeds I follow (right-hand-side column of my Links page) has steadily fallen more in line with the 6 reasons I mentioned above. Of course, the list could always use some pruning/adjusting (and as anyone who’s seen how much I share over Google Reader or on Twitter, they can tell I have a lot that I could cut from my list), but I think this set of 6 criteria is as good as any for helping people to manage their information sources.

What other criteria do people use in finding good sources of information/news to follow?

(Image credit – cover 1) (Image credit – cover 2) (Image credit – cover 3)


United States of Amoeba

Another month, another paper to read and blog about.

Most people know that viruses are notoriously tricky disease-causing pathogens to tackle. Unlike bacteria which are completely separate organisms, viruses are parasites which use a host cell’s own DNA-and-RNA-and-protein producing mechanisms to reproduce. As a result, most viruses are extremely small, as they need to find a way into a cell to hijack the cell’s  machinery, and, in fact, are oftentimes too small for light microscopes to see as beams of light have wavelengths that are too large to resolve them.

However, just because most viruses are small, doesn’t mean all viruses are. In fact, giant Mimiviruses, Mamaviruses, and Marseillesviruses have been found which are larger than many bacteria. The Mimivirus (pictured below), for instance, was so large it was actually identified incorrectly as a bacteria at first glance!


Little concrete detail is known about these giant viruses, and there has been some debate about whether or not these viruses constitute a new “kingdom” of life (the way that bacteria and archaebacteria are), but one thing these megaviruses have in common is that they are all found within amoeba!

This month’s paper (HT: Anthony) looks into the genome of the Marseillesvirus to try to get a better understanding of the genetic origins of these giant viruses. The left-hand-side panel of picture below is an electron micrograph of an amoeba phagocytosing Marseillesvirus (amoeba, in the search for food, will engulf almost anything smaller than they are) and the right-hand-side panel shows the virus creating viral factories (“VF”, the very dark dots) within the amoeba’s cytoplasm. If you were to zoom in even further, you’d be able to see viral particles in different stages of viral assembly!

Ok, so we can see them. But just what makes them so big? What the heck is inside? Well, because you asked so nicely:

  • ~368000-base pairs of DNA
    • This constitutes an estimated 457 genes
    • This is much larger than the ~5000 base pair genome of SV40, a popular lab virus, the ~10000 base pairs in HIV, the ~49000 in lambda phage (another scientifically famous lab virus), but is comparable to the genome sizes of some of the smaller bacterium
    • This is smaller than the ~1 million-base pair genome of the Mimivirus, the ~4.6 million of E. coli and the ~3.2 billion in humans
  • 49 proteins were identified in the viral particles, including:
    • Structural proteins
    • Transcription factors (helps regulate gene activity)
    • Protein kinases (primarily found in eukaryotic cells because they play a major role in cellular signaling networks)
    • Glutaredoxins and thioredoxins (usually only found in plant and bacterial cells to help fight off chemical stressors)
    • Ubiquitin system proteins (primarily in eukaryotic cells as they control which proteins are sent to a cell’s “garbage collector”)
    • Histone-like proteins (primarily in eukaryotic cells to pack a cell’s DNA into the nucelus)

As you can see, there are a whole lot of proteins which you would only expect to see in a “full-fledged” cell, not a virus. This begs the question, why do these giant viruses have so many extra genes and proteins that you wouldn’t have expected?

To answer this, the researchers ran a genetic analysis on the Marseillesvirus’s DNA, trying to identify not only which proteins were encoded in the DNA but also where those protein-encoding genes seem to come from (by identifying which species has the most similar gene structure). A high-level overview of the results of the analysis is shown in the circular map below:

The outermost orange bands in the circle correspond to the proteins that were identified in the virus itself using mass spectrometry. The second row of red and blue bands represents protein-coding genes that are predicted to exist (but have yet to be detected in the virus; its possible they don’t make up the virus’s “body” and are only made while inside the amoeba, or even that they are not expressed at all). The gray ring with colored bands represents the researchers’ best guess as to what a predicted protein-coding gene codes for (based on seeing if the gene sequence is similar to other known proteins; the legend is below-right) whereas the colored bands just outside of the central pie chart represents a computer’s best determination of what species the gene seems to have come from (based on seeing if the gene sequence is similar to/the same as another specie’s; the legend is below-left).

Of the 188 genes that a computational database identified as matching a previously characterized gene (~40% of all the predicted protein-coding genes), at least 108 come from sources outside of the giant viruses “evolutionary family”. The sources of these “misplaced” genes include bacteria, bacteria-infecting viruses called bacteriophages, amoeba, and even other eukaryotes! In other words, these giant viruses were genetic chimeras, mixed with DNA from all sorts of creatures in a way that you’d normally only expect in a genetically modified organism.

As many viruses are known to be able to “borrow” DNA from their hosts and from other viruses (a process called horizontal gene transfer), the researchers concluded that, like the immigrant’s conception of the United States of America, amoebas are giant genetic melting pots where genetic “immigrants” like bacteria and viruses comingle and share DNA (pictured below). In the case of the ancestors to the giant viruses, this resulted in viruses which kept gaining more and more genetic material from their amoeboid hosts and the abundance of bacterial and virus parasites living within.

This finding is very interesting, as it suggests that amoeba may have played a crucial role in the early evolution of life. In the same way that a cultural “melting pot” like the US allows the combination of ideas from different cultures and walks of life, early amoeba “melting pots” may have helped kickstart evolutionary jumps by letting eukaryotes, bacteria, and viruses to co-exist and share DNA far more rapidly than “regular” natural selection could allow.

Of course, the flip side of this is that amoeba could also very well be allowing super-viruses and super-bacteria which could one day wipe out the human race to breed… but, maybe I’m just being paranoid. 🙂

Paper: Boyer, Mickael et al. “Giant Marseillevirus highlights the role of amoebae
as a melting pot in emergence of chimeric microorganisms.” PNAS 106, 21848-21853 (22 Dec 2009) – doi:10.1073/pnas.0911354106

(Image Credit – Mimivirus – Wikipedia) (Figures 1, 2, and 5 from paper)


Grand Challenges

Over at Bench Press, my buddy Anthony posted about the American Association for the Advancement of Science’s collaboration with the White House and Expert Labs to help identify “which scientific and technological challenges should be the focus of policy initiatives in the coming years.” The collaboration is unique in that, to my knowledge, it is the first time (or at least one of the first times) the federal government has used social media/crowdsourcing to help shape science policy.

While my first reaction was “we’re so screwed that the White House is using Twitter/Facebook to figure out our future science policy!?”, I felt it would be fun to participate in my own little way via this blog post (even though the deadline for submission was technically April 15, I’m hoping the non-140-character-limited nature of this blog post carries some weight! :-)).

So, without further ado, here would be my list of ten things (all super-broad and super-idealistic, of course), in no particular order:

  • Enabling medical treatments to be tailored for an individual patient’s history, age, gender, and genetics
  • Safer, more precisely targeted treatments which don’t damage or affect cells they are not supposed to
  • New chemical, physical, or biological processes to more cheaply produce drugs and other chemicals
  • Advanced energy storage capable of at least an order of magnitude better energy density than existing Lithium ion batteries
  • Chemical, physical, or biological methods to capture carbon dioxide and handle the increasing amounts of pollution people are generating
  • An improved understanding of the complex systems which govern our world through new mathematical/computational techniques for approximating NP-complete problems and calculating/understanding non-linear partial differential equations
  • Petaflops-capable supercomputers which cost as much and consume as much energy as a laptop today
  • (Partially inspired by Star Trek) Intelligent natural language processing so that computers can actually understand and translate language
  • (Partially inspired by Star Trek) General-purpose scanning device capable of quickly detecting chemicals, sounds, and forms of radiation as well as performing simple tomography scans (via ultrasound and/or some other form of low-energy radiation scanning)
  • (Partially inspired by Star Trek) Near-light-speed space travel to explore beyond the solar system and allow humans to move beyond near Earth orbit

Picking ten was actually pretty difficult. There are clearly many other important scientific questions to be answered, but these were my ten. What would be on your list?

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Collateral Damage by Mitochondria

Another month, another paper to read and blog about.

This month, I read a paper (HT: my ex-college roommate Eric) by a group from Beth Israel about systemic inflammatory response syndrome (SIRS) following serious injury. SIRS, which is more commonly understood/found as sepsis, happens when the entire body is on high “immune alert.” In the case of sepsis, this is usually due to an infection of some sort. While an immune response may be needed to control an internal infection, SIRS is dangerous because the immune system can cause a great deal of collateral damage, resulting in potentially organ failure and death.

Whereas an infection has a clear link to sepsis, the logic for why injury would cause a similar immune response was less clear. In fact, for years, the best hypothesis from the medical community was that injury would somehow cause the bacteria which naturally live in your gut to appear where they’re not supposed to be. But this explanation was not especially convincing, especially in light of injuries like burns which could still lead to SIRS but which didn’t seem to directly affect gut bacteria.image

Zhang et al, instead of assuming that some type of  endogenous bacteria was being released following injury, came up with an interesting hypothesis: it’s not bacteria which is triggering SIRS, but mitochondria. A first year cell biology student will be able to tell you that mitochondria are the parts of eukaryotic cells (sophisticated cells with nuclei) which are responsible for keeping the cell supplied with energy. A long-standing theory in the life science community (pictured above) is that mitochondria, billions of years ago, were originally bacteria which other, larger bacteria swallowed whole. Over countless rounds of evolution, these smaller bacteria became symbiotic with their “neighbor” and eventually adapted to servicing the larger cell’s energy needs. Despite this evolution, mitochondria have not lost all of their (theorized) bacterial ancestry, and in fact still retain bacteria-like DNA and structures. Zhang et al’s guess was that serious injuries could expose a mitochondria’s hidden bacterial nature to the immune system, and cause the body to trigger SIRS as a response.

Interesting idea, but how do you prove it? The researchers were able to show that 15 major trauma patients with no open wounds or injuries to the gut had thousands of times more mitochondrial DNA  in their bloodstream than non-trauma victims. The researchers were then able to show that this mitochondrial DNA was capable of activating polymorphonuclear neutrophils, some of the body’s key “soldier” cells responsible for causing SIRS.

The figure above shows the result of an experiments illustrating this effect looking at the levels of a protein called p38 MAPK which gets chemically modified into “p-p38” when neutrophils are activated. As you can see in the p-p38 row, adding more mitochondrial DNA (mtDNA, “-” columns) to a sample of neutrophils increases levels of p-p38 (bigger, darker splotch), but adding special DNA which blocks the neutrophil’s mtDNA “detectors” (ODN, “+” columns) seems to lower it again. Comparing this with the control p38 row right underneath shows that the increase in p-p38 is likely due to neutrophil activation from the cells detecting mitochondrial DNA, and not just because the sample had more neutrophils/more p38 (as the splotches in the second row are all roughly the same).

Cool, but does this mean that mitochondrial DNA actually causes a strong immune response outside of a test tube environment? To test this, the researchers injected mitochondrial DNA into rats and ran a full set of screens on them. While the paper showed numerous charts pointing out how the injected rats had strong immune response across multiple organs, the most striking are the pictures below which show a cross-section of a rat’s lungs comparing rats injected with a buffer solution (panel a, “Sham”) and rats injected with mitochondrial DNA (panel b, MTD). The cross-sections are stained with hematoxylin and eosin which highlight the presence of cells. The darker and “thicker” color on the right shows that there are many more cells in the lungs of rats injected with mitochondrial DNA – most likely from neutrophils and other “soldier cells” which have rushed in looking for bacteria to fight.

Amazing isn’t it? Not only did they provide part of the solution to the puzzle of injury-mediated SIRS (what they used to call “sterile SIRS”), but lent some support to the endosymbiont hypothesis!

Paper: Zhang, Qin et al. “Circulating Mitochondrial DAMPs Cause Inflammatory Responses to Injury.” Nature 464, 104-108 (4 March 2010) – doi:10.1038/nature08780

(Image credit) (Figure 3 and 4 from paper)


A Case Fit for House MD Part 2

A little over two years ago, I blogged on a very interesting New England Journal of Medicine paper about a bizarre medical case where a young female patient actually took on the blood type of a little boy who’s liver she had taken in a transplant. I had noted then that such an amazing (and not fully-understood) event definitely qualified for being a House MD moment, after one of my favorite TV shows about everyone’s favorite misanthropic genius doctor.

Two years later, a friend of mine from college shows me another case with a similar “signature”, making me dub this “A Case Fit for House MD Part 2”!

The setup (more details in Wikipedia): a 52-year-old woman named Karen Keegan was in need of a kidney transplant and, of course, tested her children for donor compatibility. What she discovered, completely rocked her world. To quote the Damn Interesting page I just linked to:

Imagine if you discovered one day that two of your three children were genetically not yours. Recriminations, marital troubles, perhaps a divorce, right? Now add a twist. What if you were these children’s mother? Suddenly the question becomes not “Who?” but rather “Huh?”

“Huh?” is right.

So, what’s the explanation for how a mother could possibly give birth to children who are genetically not matched to her? The current theory is chimerism.

imageThe type of  biological chimerism, named after the mythical chimera which had the parts of a lion, snake, and goat all in one (see image on the right), we usually see involves an organism having DNA from multiple species. This is usually something more mundane and research/medicine-oriented like creating mice that have genes which give them a human being’s immune system. These “humanized” mice are then used to produce human antibodies which can then be used for medicinal purposes.

A more dramatic example in nature would be the parasitic chimerism that the Ceratioid Anglerfish practices – where the males of the species actually fuse with females to become some sort of chimeric (and immediately fertile) hermaphrodite.

In humans, a common form of chimerism that is observed is in a small proportion of fraternal twins where, because of linkages between their blood supply and blood-producing organs,end up having “shared blood”. They each have and will continue to produce blood cells from their other twin, despite the rest of their body being genetically distinct.

But what about the curious case of our mother who’s kids don’t appear to be hers? What sort of chimerism explains this? A New England Journal of Medicine paper dives into the science, but basically, the theory is that Karen Keegan had a fraternal twin. But, rather than simply share blood cells/blood-producing cells, Keegan and her twin had actually fused in the womb. This theory was supported when they found two sets of DNA in her tissues (one set of which matched her un-matching children).

Interestingly, this paper was cited in the 2002 trial of a British woman named Lydia Fairchild who was denied custody of her children and welfare support because she could not prove with a genetic test that she was the mother of her children. The story was later put into a documentary called “I Am My Own Twin”.

So, anyone want to pitch using this to House MD?

(Edit: It’s been brought to my attention by… pretty much all of my friends who watch House that genetic chimerism was actually the diagnosis for the second episode of season 3 — I suppose I won’t be able to sell this screenplay to the writers after all…)

(Image credit)


Slime takes a stroll

It was the end of February yesterday – which means its time to read/blog about another paper!

The paper I read for this month brought up an interesting question I’ve always had but never really dug into: how do individual cells find things they can’t “see”? After all, there are lots of microbes out there who can’t always see where their next meal is coming from. How do they go about looking?

A group of scientists at Princeton University took a stab at the problem by studying the motion of individual slime mold amoeba (from the genus Dictyostelium) and published their findings in the (open access) journal PLoS ONE.

As one would imagine, if you have no idea where something is, your path to finding it will be somewhat random. What this paper sought to discover is what kind of random motion do amoeboid-like cells use? To those of you without the pleasure of training in biophysics or stochastic processes, that may sound like utter nonsense, but suffice to say physicists and mathematicians have created mathematically precise definitions for different kinds of “random motion”.

Now, if the idea of different kinds of randomness makes zero sense to you, then the following figure (from Figure 1 in the paper) might be able to help:


Panel A describes a “traditional” random walk, where each “step” that a random walker takes is completely random (unpredictable and independent of the motion before it). As you can see, the path doesn’t really cover a lot of ground. After all, if you were randomly moving in different directions, you’re just as likely to move to the left as you are to move to the right. The result of this chaos is that you’re likely not to move very far at all (but likely to search a small area very thoroughly). As a result, this sort of randomness is probably not very useful for an amoeba hunting for food, unless for some reason it is counting on food to magically rain down on its lazy butt.

Panel B and C describe two other kinds of randomness which are better suited to covering more ground. Although the motion described in panel B (the “Levy walk”) looks very different from the “random walk” in Panel A, it is actually very similar on a mathematical/physical level. In fact, the only difference between the “Levy walk” and the “random walk” is that, in a “normal” random walk, the size of each step is constant, whereas the size of each “step” in a “Levy walk” can be different and, sometimes, extremely long. This lets the path taken cover a whole lot more ground.

A different way of using randomness to cover a lot of ground is shown in Panel C where, instead of taking big steps, the random path actually takes on two different types of motion. In one mode, the steps are exactly like the random walk in Panel A, where the path doesn’t go very far, but “searches” a local area very thoroughly. In another mode, the path bolts in a straight line for a significant distance before settling back into a random walk. This alternation between the different modes defines the “two-state motion” and is another way for randomness to cover more ground than a random walk.

And what do amoeba use? Panel D gives a glimpse of it. Unlike the nice theoretical paths from Panels A-C rooted around random walks and different size steps or different modes of motion, the researchers found that slime mold amoeba like to zig-zag around a general direction which seems to change randomly over the course of ~10 min. Panel A of Figure 2 (shown below) gives a look at three such random paths taken over 10 hours.


The reason for this zig-zagging, or at least the best hypothesis at the time of publication, is that, unlike theoretical particles, amoeba can’t just move in completely random directions with random “step” sizes. They move by “oozing” out pseudopods (picture below), and this physical reality of amoeba motion basically makes the type of motion the researchers discussed more likely and efficient for a cell trying to make its way through uncharted territory.


The majority of the paper actually covers a lot of the mathematical detail involved in understanding the precise nature of the randomness of amoeboid motion, and is, frankly, an overly-intimidating way to explain what I just described above. In all fairness, that extra detail is more useful and precise in terms of understanding how amoeba move and give a better sense of the underlying biochemistry and biophysics of why they move that way. But what I found most impressive was that the paper took a very basic and straightforward experiment (tracking the motion of single cells) and applied a rigorous mathematical and physical analysis of what they saw to understand the underlying properties.

The paper was from May 2008 and, according to the PLoS One website, there have been five papers which have cited it (which I have yet to read). But, I’d like to think that the next steps for the researchers involved would be to:

  1. See how much of this type of zig-zag motion applies to other cell types (i.e., white blood cells from our immune system), and why these differences might have emerged (different cell motion mechanisms? the need to have different types of random search strategies?)
  2. Better understand what controls how quickly these cells change direction (and understand if there are drugs that can be used to modulate how our white blood cells find/identify pathogens or how pathogens find food)

(All figures from paper) (Image of Pseudopod)

Paper: Li, Liang et al. “Persistent Cell Motion in the Absence of External Signals: a Search Strategy for Eukaryotic Cells.” PLoS ONE 3 (5): e2093 (May 2008) – doi:10.1371/journal.pone.0002093


Crazy Y Chromosomes

A few weeks ago, I set myself some 2010 goals. One of which was to make sure that I fit in reading at least one paper every month. What I didn’t say though, was that I would try to do a quick blog post on each (to help keep me honest).

I forgot exactly how I found this paper, but the subject immediately caught my eye:

Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content

What? I had always been taught that the genomic differences between chimpanzees and humans were extraordinarily small, and since I’m male, I was also drawn to the fact that it would talk about a chromosome that was very near and dear to me.

What I read was pretty amazing. Despite the fact that we are very genetically similar to chimpanzees the Y chromosomes of our two species are actually very different. The best depiction of this that I can point to is from Figure 2 of the paper (below). The two charts below are dot plots which show where the human and chimpanzee chromosomes “line up”, so to speak. The right-hand chart shows how closely related the human chromosome 21 is to the analogous chimpanzee chromosome. You can see this from the nearly perfect diagonal line, showing that the two chromosomes are pretty close to identical as you move from one end of the chromosome to the other. The left-hand chart shows a similar comparison of a human Y chromosome and a chipmanzee Y chromosome. Notice the difference?


While it was fascinating to read what specifically was different (i.e. repeats, ectopic homologous recombination, introduction of nonsense mutations and open reading frames), what I found most interesting was the speculation as to why the Y chromosomes of two very similar species would diverge so much in such a narrow period of time. The research group’s hypothesis is that the Y chromosome holds a great deal of influence over sperm production, and because a Y chromosome will never have a “partner” chromosome the way that every other non-sex-determining chromosome does, changes in the Y chromosome are likely to have very significant changes in sperm characteristics. Because female chimpanzees oftentimes mate with multiple males, there is strong sperm competition and hence strong selective pressure for chimpanzees to have rapid evolution in the Y chromosome.

Of course, this is all just a guess. One way to test it would be to compare the human Y chromosome sequence with further primate species and see if primates where sperm competition is less intense have more similar chromosomes as humans. Another would be to see if any of the genetic changes resulted in clear sperm/testes genetic or transcriptional control differences.

But, all in all, a very cool start to what I’m hoping will be a fun 12 months!

(Figure 2 from paper)

Paper: Hughes, Jennifer F. et al. “Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content.” Nature 463, 536-539 (28 January 2010) – doi:10.1038/nature08700


Bet on chance

When people think about strategy, they’re oftentimes looking for that one “silver bullet” which is the 100% correct and best answer. This is despite the fact that it is sometimes 100% valid to use random chance to make a decision.

Well, it turns out that bacteria have figured this out as well, as researchers have recently reported in Nature (HT: Wired Science). The researchers did a fascinating experiment where they forced bacteria to cope with a rapidly changing environment. Normally, you would expect that, if bacteria were forced into a different environment, the population as a whole would “evolve” to acquire the traits that are necessary to survive in that environment. And, at first, this is what the researchers observed – the shifts in environment “drove the successive evolution of novel phenotypes by mutation and selection.”

imageBut, after a while, something very interesting happened – some of the bacterial populations (roughly 1 in 12) “recognized” that they were being put through the ringer and evolved a “gambling” strategy (the researchers called it a “stochastic switching between phenotypic states”) whereby individual bacteria would actually pick a strategy at random! “Knowing” that they were in a constant state of environmental flux with little predictability, these populations of bacteria evolved an ability to have individual bacterium pick random strategies such that genetically identical bacterium would end up with very different traits!

Many people, let alone bacteria, find the idea of a random strategy as a winning one to be counter-intuitive. But, the ability of even the simplest creatures to re-capitulate proves that randomness can not only be effective, but its possibly how the earliest living things coped with a very strange and rapidly changing environment.

(Image credit)

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An electric eel’s version of Energy Star

It never ceases to amaze me the extent to which nature beats man to the punch when it comes to coming up with innovative solutions. There’s a reason, after all, that so much of engineering is biomimicry.

image One cool example of nature coming up with a solution to a problem humans rea dealing with is something I recently encountered is from a journal article from the open access journal PLoS Biology (meaning that you don’t need to pay to read the article) on electric fish. While most people think of electric eels which are known to stun prey with electrical discharges when they think of electric fish, but there are many species of electric fish which use weaker types of electrical discharges for navigating (“electroclocation” – like echolocation, but with electricity) or communication.

Just like humans eventually did, electric fish have discovered that … electricity is costly to produce. These electric fish might not pay dollars and cents for said electricity, but they pay for it in terms of calories (they need to consume extra food to sustain their electrical abilities) and, for some species, in terms of being easily detected by electroreceptive predators (predators who can detect electrical fields).

A team of researchers at UT Austin and Florida International University studied a particular species of electric fish – the longtail knifefish (Sternopygus macrurus) and found that they were able to lower the strength of their emitted electrical fields by ~40%! This lowering of “power consumption” (to misuse the term) was triggered to changes in the day (these electric fish are more active at night, so they turn it up when the sun goes down and turn it down when the sun comes up) and when they were being social.

This, in turn, was all found to be controlled by a hormonal system that is analogous to the biological clock that controls when you or I feel like we need to sleep or wake up. These hormones triggered a change in the sodium channel proteins (like the ones that transmit our brain signals through our nerves) which moved them from their active position to an inactive position, increasing or lowering the knifefish’s electrical output.

I’ll leave those more interested in the biological details to check out the paper (which is very readable, even for novices), but I only hope that it takes humans less than the millions of years evolution that the longtail knifefish needed to solve its energy problems. After all, all we need is some sort of hormonal system (Higher prices at different times of the day? Smart grid signals?) that pushes our power consumption (Electronics which have different levels of power consumption, kind of like what some of today’s chips have? Maybe adaptive lighting/cooling/heating? Smart grid technology?) to different levels…

Paper: Markham MR, McAnelly ML, Stoddard PK, Zakon HH (2009) Circadian and Social Cues Regulate Ion Channel Trafficking. PLoS Biol 7(9): e1000203. doi:10.1371/journal.pbio.1000203

(Image credit – Wikipedia)

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Why Comics? Why SciFi?

There’s no denying it. Comic books and science fiction have more than their fair share of “only for geeks.” While I would be hard pressed to deny who I am, I will say that my love for science fiction goes far beyond just pure escapism.

imageNow, I could talk about how I think comic books represent a reassuring world where the good guys triumph and where the human spirit and concepts of justice and loyalty are all that is necessary to be a hero, and how I believe that science fiction represents an optimism about the future and the importance of human emotions and morals. But instead of “taking my word for it”, why not hear Reading Rainbow host and the actor behind Star Trek’s Geordi LaForge LeVar Burton take on the subject (yes, the quotes were an intentional Reading Rainbow reference):

I’m one of those people that believes that there was some kid back in the 1960s watching Star Trek, and he kept seeing Captain Kirk pull out this communicator and flip it open – and that kid grew up and became an engineer, a designer of products, and we now have a device that is more common than the toaster. How many flip phones do you see on a daily basis? That which we imagine is what we tend to manifest in third dimension –  that’s what human beings do, we are manifesting machines.  The metaphor of a man who has an external electronic device, something man-made that serves him and somehow serves humanity, and that he becomes so aligned with that device, with the power of that device, that at one point he can discard it – I think that’s a real metaphor for the human journey. One day we won’t need a transporter device to get from one place to another.  And it begins with the wheel and then migrates through airplanes to some future technology that we can’t produce yet but we can imagine.  Imagination is really the key part of the human journey, it’s the key to the process of manifesting what our heart’s desire is.

When I was a kid, it was comic books that pointed me in that direction and from comic books I went to science fiction literature, which is still one of my most favorite genres of literature to read.  Don’t underestimate the power of comics and what they represent for us and how they inform us on the journey of being human – because it’s powerful. It’s very powerful. They give us permission to contemplate what’s possible. And in this world, in this universe, there’s nothing that is not possible.  If you can dream it, you can do it.

To many African-Americans, like Burton and fellow Star Trek actor/fan Whoopi Golderg, Star Trek holds a very special role in their minds:

imageWhen I was a kid, I read a lot of science fiction books and it was rare for me to see heroes of color in the pages of those novels.  Gene Roddenberry had a vision of the future, and Star Trek was one that said to me, as a kid growing up in Sacramento, California, “When the future comes, there’s a place for you.”  I’ve said this many times, and Whoopi (Goldberg) feels the same way – seeing Nichelle Nichols on the bridge of the Enterprise meant that we are a part of the future.  So I was a huge fan of the original series and to have grown up and become of that mythos, a part of that family, and to represent people dealing with physical challenges, much like what Nichelle Nichols represented for people like Whoopi and myself, I can’t even begin to share with you what that means to me.

While I was fortunate enough to be born in an era where nobody questions the role of Asian-Americans in industry and science, I can also see why many Asian-Americans would have been similarly inspired by George Takei’s role as Sulu in the original Star Trek series.

(Interview on LeVar Burton’s upcoming role in DC’s Superman/Batman: Public Enemies DVD) (Image Credit – LeVar Burton) (Image Credit – Nichelle Nichols)

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Wolfram|Alpha reaches out to students

In educational circles, there’s always a philosophical debate between those educators who favor allowing their students to use tools like TI-89’s or computer algebra-capable software like Mathematica and those who don’t, with those favoring their use citing the ability of the tools to expand the scope of the curriculum, and with those opposed worried about the tools supplanting the instincts that long practice engenders.

I personally am in favor of using such tools, as they allow a classroom to extend beyond simply learning how to do basic procedures to looking at real-world problems which are far harder and far more interesting than the simple “toy problems” which classrooms requiring all work to be done “old school” are limited to. But, even I have to say that the latest blog post by Wolfram|Alpha makes this supporter of new technical tools in classrooms a little wary.

Over on the Bench Press blog, we’ve posted a couple of times on the power of the new “computational knowledge engine” Wolfram|Alpha (brought to you by the makers of Mathematica) and its ability to help provide contextual medical and astronomical information, in addition to answers to sophisticated Mathematica queries.

Now, this should raise the eyebrows of any teacher who finds him/herself wondering if his/her students are “cheating” with computer algebra systems. And, what will raise their eyebrows even further is Wolfram’s latest post entitled, “College is Hard. Wolfram|Alpha makes it easier.

I kid you not. Have problems balancing equations in chemistry? Just have Wolfram|Alpha do it:


Need to calculate a Taylor Series? Have Wolfram|Alpha do it:


I find myself asking – why didn’t I have this when I was in college?

(Image credits – Wolfram|Alpha blog)

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Everything You Want to Know About Antigen Processing

It’s been a while since I’ve worked in a lab, but I remembered always being fascinated by the “tell all” posters which were on the lab walls which laid out everything in a cell/system pertaining to a specific concept in biology. What appealed to me about them is that they conveyed a the complex and interconnected pieces which only together made life work. It was very awe-inspiring (as well as a quick cheat sheet when I had to pretend like I knew what I was researching).

It’s been a while since I’d seen one, but thankfully, Ian York of Michigan State University and blogger at Immunology blog Mystery Rays from Outer Space linked to a new poster from Nature which reviews what is currently know about antigen processing/presentation (translation: how our cells recognize hostile bacteria/viruses/fungi/etc and alert the immune system to them).

Check it out:



(Credit – Nature Reviews Immunology)

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It’s just a little bit of G-T-C-A…

I may never run another molecular biology reaction in my life, but if I do, I will probably push my lab to buy a PCR machine from Bio-Rad .

First, my college roommate and Benchpress-partner Eric pointed me to this amazing video a couple of months ago:

Flash forward a few months and Eric points me to the sequel (no you’re not seeing things, I said “sequel”):

Now come on, Roche. Let’s see some more competition!

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Eternal youth

The “holy grail” of aging research is the ability to actually reverse the aging process. Or in other words, turn the clock back on this aged fellow on the left and transform him back into the handsome young thing on the right:

Of course, as with all things biological, nature figured this out long before any pharmaceutical/cosmetics company or scientist did. The creepy thing though, is that the solution nature came up with comes in the form of a jellyfish. An immortal jellyfish.

Turritopsis nutricula has a magical gift which countless celebrities would kill for — it has the ability to become young after each round of mating. As far as I know, no other species can do this, and as far as scientists can tell — this little jellyfish can “become young again” (as in return to its “juvenile” polyp form) as many times as it wants.

The consequence? It’s spreading like a cancer — where it once was only in the Caribbean, it’s now everywhere. Imagine if Paris Hilton never died because she never aged. But, she kept reproducing. Yeah, that’s how intense this is.

So, pick how you want the world to end:

collision with an asteroid in 2036
black hole from the Large Hadron Collider
– or invasion of immortal unstoppable jellyfish creatures

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From Slate (HT: Marginal Revolutions):

The world of scientists remains distant and bizarre to most Americans. Only 18 percent of Americans know a scientist personally, according to a 2005 survey (subscription required), and when asked in 2007 to name scientific “role models,” the results were dismal. Forty-four percent of Americans couldn’t come up with a name at all, and among those few who did, their top answers were either not scientists or not alive: Bill Gates, Al Gore, Albert Einstein.

Its a tragedy that, despite living in a society that depends so much on science and technology for its wealth and position in the world, there are a surprising number of Americans who pay it little attention and an even larger group of people who seem woefully uneducated about it.

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SUND-ay terror

I’m a big fan of House, not only because the lead character is someone we all (or maybe just me) wish we could be (someone so brilliant that he can get away with saying and doing just about anything), but because of their use of bizarre medical cases showing off some of the extreme things that one’s body is capable of when sick.

While SUND (Sudden Unexplained Nocturnal Death) will probably never show up on House (given the sudden, inexplicable death of the patient preventing House and company from being able to do or say much of anything), it is definitely one example of an extremely bizarre condition which doctors still don’t have a good handle on.

I first read about it in an article on Forbes covering bizarre sleep disorders. The craziest thing about this “condition” is that it seems the victims die of nightmares!?:

Since 1977, more than a hundred Southeast Asian immigrants in the U.S., primarily ethnic Hmong from Laos, have died from a mysterious disorder known as Sudden Unexpected Nocturnal Death Syndrome, according to reports by the U.S. Center for Disease Control. The victims were mostly imagemen in their 30s or older, who were apparently in good health when they died in their sleep for no apparent reason.

“The victim has no known antecedent illnesses, and there are no factors  that might precipitate cardiac arrest,” the Cambridge History of Disease notes. “At autopsy, no cause of death can be identified in the heart, lung or brain. Postmortem toxicologic screening tests reveal no poisons.”

Shelley Adler, a professor of integrative medicine at the University of San Francisco, California School of Medicine, speculates that the cataclysmic psychological stress caused by war, migration and rapid acculturation created such wrenching nightmares among Hmong refugees that they died. In other words, nightmares killed them.

Doing some additional research on Wikipedia reveals that the current operating hypothesis appears to be cardiovascular – mainly that SUNDS victims could all have potentially died of ventricular fibrillation (a lethal heart arrhythmia where the heart ceases to pump normally). There’s even a syndrome named for this – Brugada syndrome – with 6 associated genes which show a higher risk for the condition.

Now, in all honesty, I’m not sure how you diagnose a patient who’s already dead (esp. when autopsies and histories reveal nothing significant), but that leads us to the prognosis:

  1. If no one you know died suddenly in their sleep, you probably won’t either (it’s at least partially genetic)
  2. If someone you know did die suddenly in their sleep, go bulk up on Thiamine (Vitamin B-1), get routine heart monitoring, and maybe get a cardiac defibrillator implanted into your chest.

On that note, happy holidays everyone!

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