Fascinating, Orbital cycles, Australian lake levels, and the arrival of aborigines:

But the other big feature is that the lake-filling events that occurred after 50,000 years ago were much smaller than those which occurred before. Climactically, the conditions 10,000 years ago should have been the same as the conditions 115,000 years ago. But the lake was only a fraction of the size. The authors find no natural causes which can explain this. So they suggest that the aridity starting around 50,000 years ago is related to the reduction in forest and increase in grasslands which occurred at this time. This vegetation change was a result of a huge increase in the frequency of fire in central Australia, which allowed fire-adapted plants to prosper at the expense of moisture-retaining forest. The increase in fire at this time is generally associated with the arrival of the first people on the Australian continent. It is known that of Australia’s megafauna went extinct at this time, but Magee et al. (2004) show that even the tropical rains were effected by human migration, with drastic changes to the continent’s largest river basin.

If you read some of the academic literature on fire ecology you have a hard time not coming to the conclusion that modern humans terraformed the planet Earth! The hallmark of modern H. sapiens seems to be extinction of large organisms, a propensity to go where no hominin has gone before, and copious utilization of the “red flower.”

Every year at this time the People’s Choice Podcast Awards are held. This year, three different podcasts with which I am involved in some way are nominated in the Science category!

Big Picture Science (what used to be Are We Alone) is the SETI podcast/radio show where I do the (roughly) monthly Brains on Vacation segment with astronomer Seth Shostak. My friends Fraser Cain and Pamela Gay do the Astronomy Cast podcast (I’ve been on it a few times). And the Skeptics Guide to the Universe podcast, where I’m a frequent guest and general rabble-rouser, is also nominated.

I like all three, so I have no problem if my readers vote for any of these. You can vote every day, once per day, until October 27. Voting resets at midnight Eastern US time.

Alexander Dumas, of mixed race

One of the reasons I post regularly on the genetics of mixed-race people and their physical appearance is that I don’t think the media does a good job. There’s a “freak show” element which titillates but does not illuminate. This in a period in the United States where the absolute number of people of mixed origin is increasing rapidly due to intermarriage. In fact for years I’ve gotten inquiries from the parents of mixed-race children about the scientific details of the genetics, because they are regularly questioned in depth as to how the children came to look how they look (the emails are always from women, more on that later). A relatively well written article in The New York Times illustrates some of the issues, insofar as the focus is totally on social context and dynamics, with not even a small nod to the science. The story is about a mixed-race woman (mother white and father black) who is married to a white man, whose children don’t “look black.” Specifically, her two daughters are very light-skinned, and the younger one is boldly blonde.

Here’s the jump off point of the piece:

“How come she’s so white and you’re so dark?”

The question tore through Heather Greenwood as she was about to check out at a store here one afternoon this summer. Her brown hands were pushing the shopping cart that held her babbling toddler, Noelle, all platinum curls, fair skin and ice-blue eyes.

The woman behind Mrs. Greenwood, who was white, asked once she realized, by the way they were talking, that they were mother and child. “It’s just not possible,” she charged indignantly. “You’re so…dark!”

It was not the first time someone had demanded an explanation from Mrs. Greenwood about her biological daughter, but it was among the more aggressive….

Of course it’s possible. The science behind this is trivially plain. The biological mother has alleles which code phenotypes distinctive of Europeans and Africans. Because her father is African American she is even likely to have more European ancestry than African ancestry (median African American is ~80% African and ~20% European). Genes which control variation in skin pigmentation at the scale of racial differences are distributed across half a dozen loci, but with blue vs. brown eye color there’s really only one locus which explains most (though not all) of the variation. That probably explains how both the daughters have blue eyes. The mother is probably a heteozygote, and the father is a homozygote. That means that any one of their children has a ~50% chance of having blue eyes and a ~50% chance of having brown eyes. So the chance of both daughters turning out to have blue eyes is ~25%. But obviously the science isn’t the meat of the piece. I just wish they’d given a quick explicit nod to it so that people would know why the outcome is as it is. It’s not rocket science.

In terms of the experiences of this family, there are a few issues that come to mind. First, it would be nice to clarify the ages of the individuals who ask her rude questions. My personal experience is that people who compliment me on my ability to speak English well have invariably been born before 1970. No matter one’s politics or current life situation formative experiences matter. These are people who grew up in the United States before there were large numbers of children in their classrooms who “didn’t look American” (i.e., they weren’t black or white). In contrast, people who are younger had some of these kids in their classes growing up, so the fact that we don’t have accents and can speak English fluently isn’t an amazing feat which requires a compliment.

Second, I wonder as to the dynamics in this specific case, a mixed-race women who is coded as black in the United States. It doesn’t seem implausible that the experiences of Asian American and Latino women who have very light-skinned children would be somewhat different, because there’s a lot less fraught history there. The power of hypodescent still looms large in black-white relations, in a way it necessarily does not with other groups.

Finally, there’s the issue of mothers versus fathers. These stories always seem to focus on mothers who are assumed to be nannies of their own children. This is a very specific fear which I’ve read some black women have when it comes to interracial dating and the “think of the children” angle. But what about the fathers? It seems that paternity is something which is going to be much more plausible to challenge. In the few cases where black American families have adopted white children I’ve read that they have to be very cautious in public lest people get the wrong impression, and this is a particular problem with black males (like some gay couples keeping adoption papers on one’s person can be handy in these instances).

But that’s all sociology. There’s a lot of moving parts. But the genetics of this isn’t too complex. Quite possible indeed.

You wouldn’t know it from crime shows, but DNA evidence can have more holes in it than Swiss cheese. And the Amanda Knox murder appeal, in which the DNA evidence that led to Knox and former-boyfriend Sollecito’s convictions in 2009 was thrown out, provided a great example of how a powerful tool, when used incompetently, can be worse than useless.

Getting a DNA fingerprint—matching a particular piece of DNA to a specific individual—is a very delicate process. Samples from the crime scene must be taken immediately, and the object they’re found on must be pristine, not touched by anyone else for quite a while. John Timmer at Ars Technica deftly explains the science behind DNA fingerprinting  and asks experts how the DNA evidence in the Knox trial, taken from the victim’s bra clasp and a knife, measures up. It ain’t pretty:

The experts were not kind to the evidence. The bra clasp, it turned out, had sat on the floor for more than six weeks after the murder before being secured and processed; photographs show that it had been moved between the murder and its eventual collection. The clasp was the only DNA evidence placing Sollecito at the scene of the crime; no DNA put Knox on the scene at all.

The supposed murder weapon, a long kitchen knife, was found in the home of Sollecito, in his kitchen knife drawer. The knife held little DNA and, according to the experts, the local authorities had not handled the tests properly to compensate.

The tiny bit of DNA on the knife produced results so spotty that they would be legally barred from being introduced in a US court. But not, evidently, an Italian one. Yeesh. Read more at Ars Technica.

Image courtesy of Kuzma / istockphoto

Last month when British papers reported on the “first Irish case of death” by spontaneous human combustion—going up in flames with no apparent cause—many eyebrows were raised in the scientific regions of the Internet. Apparently the coroner in the case had never heard of the “wick effect,” in which a flaming object like a cigarette dropped on a sleeping person can slowly melt all their (quite flammable) fat until it leaks out and saturates the body, forming, in effect, a human candle or torch. It’s what forensic scientists think happens in cases of so-called “spontaneous” human combustion.

Blogger Jennifer Ouellette, it turns out, is a font of knowledge on the wick effect and the various other explanations people have come up with over the years for the gruesome discovery of a pair of legs leaning against a chair full of ash and grease. Dickens, along with the rest of the Victorians, thought it happened because of heavy drinking. But these explanations really take the cake:

A man named John Heymer wrote a book called The Entrancing Flame in 1996, in which he advanced his hypothesis that SHC victims are loners who fall into a strange kind of trance that triggers a chain reaction of “mitochrondrial explosions” by “freeing hydrogen and oxygen within the body.” That hypothesis might make sense if hydrogen and oxygen actually existed in gas form inside a mitochrondrial cell, but they don’t — and a good thing, too, otherwise the very act of inhaling could cause spontaneous ignition.

Even more far-fetched is the take of a man named Larry Arnold, who thinks that occasionally human cells get hit by a mysterious particle — he calls it a “pyrotron” — that causes a nuclear chain reaction inside the body. We give Arnold points for creativity and coming with a really cool moniker for his imaginary new particle.

Read more at Cocktail Party Physics.

Image courtesy of puzzledmonkey / flickr

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Take a look at the image displayed here [click to redshiftenate]. Every object you see there is a galaxy, a collection of billions of stars. See that one smack dab in the middle, the little red dot? The light we see from that galaxy traveled for 12.9 billion years before reaching the ESO’s Very Large Telescope in Chile. And when astronomers analyzed the light from it, and from a handful of other, similarly distant galaxies, they were able to pin down the timing of a pivotal event in the early Universe: when the cosmic fog cleared, and the Universe became transparent.

This event is called reionization, when radiation pouring out of very young galaxies flooded the Universe and stripped electrons off of their parent hydrogen atoms. An atom like this is said to be ionized. Before this time, the hydrogen gas was neutral: every proton had an electron around it. After this: zap. Ionized. This moment for the Universe was important because it changed how light flowed through space, which affects how we see it. The critical finding here is that reionization happened about 13 billion years ago, and took less time than previously thought, about 200 million years. Not only that, the culprit behind reionization may have been found: massive stars.

OK, those are the bullet points. Now let me explain in a little more detail.

Young, hot, dense, and chaotic

Imagine the Universe as it was 13.7 billion years ago. A thick, dense soup of matter permeates space, formed in the first three minutes after the Big Bang. The Universe was expanding, too, and cooling: as it got bigger, it got less dense, so the temperature dropped. During this time, electrons and protons were whizzing around on their own. Any time an electron would try to bond with a proton to form a neutral hydrogen atom, a high-energy photon (a particle of light) would come along and knock it loose again.

During this period, the Universe was opaque. Electrons are really good at absorbing photons, so light wouldn’t get far before being sucked up by an electron. But over time, things changed. All those photons lost energy as things cooled. Eventually, they didn’t have enough energy to prevent electrons combining with protons, so once an electron got together with a proton they stuck together. Neutral hydrogen became stable. This happened all over the Universe pretty much at the same time, and is called recombination. It occurred about 376,000 years after the Big Bang.

When this happened, the Universe became transparent to visible light because neutral hydrogen is really bad at absorbing the kind of light we see. However, it’s really good at absorbing ultraviolet light, and that’s the key to our story. Up until this point, there were no stars, no galaxies. But over time, hundreds of millions of years, the gas and dark matter in the Universe clumped up, attracted by their mutual gravity, and started forming galaxies and stars. Some of these stars were massive, hot, and bright, and flooded the sky with ultraviolet light.

This UV was then promptly absorbed by the neutral hydrogen out in space. If the UV photons had enough energy, kablam! They’d blow an electron right off its hydrogen atom, ionizing it. For hundreds of millions of years, the universe was neutral, but then those pesky stars fired up, and started ionizing it again. That’s why we call this reionization.

Not only that, but all this time the Universe was still expanding. As it did, it got less dense, the matter spreading out more thinly over space. Once the stars started ionizing the hydrogen, the average distance between the electrons and protons was getting big enough that it was tough for them to recombine (and if they did, along came another UV photon, pinging off the electron again). Between the flood of UV light and the cosmic expansion, the Universe stayed ionized. It was such an efficient process that today, 13 billion years later, the Universe is still mostly ionized. Neutral hydrogen is pretty rare compared to its ionized brethren.

A long time ago, in a bunch of galaxies far, far away…

And that’s where these new results (PDF) come in. The astronomers studied a handful of galaxies at different distances. They are so far away that the light we see from them was emitted around the time of reionization. By looking at the amount of ultraviolet we see from these galaxies, we can determine how much neutral hydrogen it passed through (since that gas absorbs the light, making the galaxy appear fainter) versus ionized gas. These galaxies were all very far away, but not exactly the same distance. Remember, it takes time for light to reach us, so we may be seeing one galaxy as it was 13 billion years ago, and another as it was 12.9 billion years. That makes a big difference! Because these galaxies were at different distances, it allowed the astronomers to see what reionization was like at different times.

Sure enough, the most distant galaxies had more of their UV light absorbed than the ones that were closer. What the astronomers found was that 780 million years after the Big Bang the Universe was mostly neutral, but only 200 million years later was mostly ionized. In other words, the flood of UV radiation managed to ionize essentially the entire Universe in only 200 million years, faster than what had previously been supposed!

Ah, now it’s all clear to me

Think about that for a moment. We are looking at objects that are so far away it takes huge telescopes just to see them at all, despite the fact that they are blasting out UV radiation at a rate that makes them billions of times brighter than the Sun. We are peering across the entire Universe to see what it was like when it was young, very young, and we’re able to actually see what it was doing, and understand it.

That’s so cool.

Not only that, but another team of astronomers independently added to this finding by solving another riddle about it. I wrote above that it was stars that reionized the Universe, but in fact that’s not the entire story. Giant black holes gobbling down matter are sloppy eaters, and as material falls in it blasts out high-energy radiation, including UV, as well. How much of that reionizing UV light was from stars, and how much from those big black holes?

[Click to galactinate.]

The other study (PDF) looked at nearby galaxies that are emitting lots of UV light, more than usual for normal galaxies, and were probably more common in the early Universe. The image above is one such galaxy, NGC 5253, as seen by the Magellan Baade 6.5 meter telescope. They found that these galaxies are undergoing bursts of star formation, and that means lots of massive, hot stars that can flood space with UV. Calculating how many stars are formed, how much UV is emitted, and extrapolating that back to the early Universe, they find that stars were the main culprit in reionizing the Universe 13 billion years ago.

That’s amazing. Stars were so plentiful and so energetic even so long ago that they were capable of ionizing the entire Universe!

The proper study of the Universe is the Universe

One thing that may be confusing (OK, a lot of this is, but one thing that stands out) is that if the Universe is currently ionized, and free electrons are so good at absorbing light, why isn’t the Universe opaque today? It’s because the Universe is so thinly spread out! Sure, electrons absorb light, but there are simply so few of them in space that your random photon from a distant galaxy has a very good chance of traveling billions of light years without getting close enough to one to impact it and get swallowed up. That’s why the Universe is transparent, and allows us to see nearly all the way across it.

So you have to consider not just that neutral hydrogen is good at absorbing UV and bad at visible light (and the opposite when it’s ionized) but also how dense it is. Way back in the olden days it was thick enough to absorb light, but now, even though it’s ionized, it’s too thin to absorb light efficiently. That happened around the same time as reionization, so once the hydrogen got zapped, it stayed zapped.

I know it’s a little confusing, but the universe is a fairly complicated place. That’s why we’re still trying to figure it out! We think the rules it obeys, the laws of nature, are actually relatively simple and elegant. But there are a lot of them, and they interact in complex ways. If they didn’t, we wouldn’t be here to study them! So really, if you think about it, we are the result of the Universe’s laws made incarnate, evolved to the point where we can study ourselves.

Image credits: ESO/ L. Pentericci; NASA/ESA/Hubble; Jordan Zastrow

In September 2011, I was honored to be on the speaker roster for TEDxBoulder, which is a local though independently-run version of the much-lauded TED talks. My talk was about saving the Earth from asteroid impacts, something I’ve spent a lot of time thinking and writing about.

The talk is online, and I’ve included it here:

The "We have a space program" line is from science fiction author Larry Niven, so I can’t take credit for it, though I modified it to add the "we can vote" bit. Also, this was the biggest audience I’ve ever spoken to, and it was a great crowd. I was almost last on the roster, but the audience was attentive and clearly enjoying themselves. It was a really fun, energizing, and mind-expanding evening.

The other talks that night are being put online as well. If you ever get a chance to attend a local TEDx conference, you should.

Beautiful faces have variable reward value: fMRI and behavioral evidence.

“The brain circuitry processing rewarding and aversive stimuli is hypothesized to be at the core of motivated behavior. In this study, discrete categories of beautiful faces are shown to have differing reward values and to differentially activate reward circuitry in human subjects. In particular, young heterosexual males rate pictures of beautiful males and females as attractive, but exert effort via a keypress procedure only to view pictures of attractive females. Functional magnetic resonance imaging at 3 T shows that passive viewing of beautiful female faces activates reward circuitry, in particular the nucleus accumbens. An extended set of subcortical and paralimbic reward regions also appear to follow aspects of the keypress rather than the rating procedures, suggesting that reward circuitry function does not include aesthetic assessment.”

Photo: flickr/indi.ca

Related content:
Discoblog: NCBI ROFL: I don’t think this explains why my passport picture sucks.
Discoblog: NCBI ROFL: Beauty week: Do hotter men have better semen?
Discoblog: NCBI ROFL: Beauty week: Beauty and the teeth.

WTF is NCBI ROFL? Read our FAQ!

Zach Weiner, of Saturday Morning Breakfast Cereal, and Kelly Smith, of Weinersmith, interviewed me for their new podcast, The Weekly Weinersmith. I am actually only their second guest, so we’ll see if the podcast survives.

We talked about the James Webb Space Telescope, mostly, though as usual when I talk to Zach we both revert to 15 year old boys. But only briefly, and only if 15 year old boys paid attention in world history class.

I’ll note I made a mistake in the interview: I said JWST will have 6 mirrors, but it actually has 18. D’oh! I remember very clearly picturing the telescope in my head (it’s hard to do a web search during an interview) and for some dumb reason I was thinking of the old MMT, which I’ll admit is a little bizarre. Heat of the moment, I guess. I wasn’t even within an astronomer’s usual factor of two, so I guess I have to give myself three geek demerits.

I think I made up for it by calling JWST — since its future is uncertain — "Schrödinger’s telescope".

In fact, the stuff I said about JWST deals mostly with its politics and budgetary woes. I’ve written about this before:

- Where will JWST’s money come from?
- The Senate has “saved” JWST? Hang on a sec, folks…
- The watershed moment for JWST
- Hubble’s successor: doomed or saved?
- Congress puts NASA and JWST on the chopping block

So there you go. I’ll note that it’s mostly wondering about JWST’s and NASA’s future until about 45 minutes in, and then we get all optimistic and fun.

Zach and Kelly were great hosts, letting me blather on until I ran out of air. Knowing them both — Kelly’s a scientist, and Zach a hugely devoted science enthusiast and supporter (he’s teaching himself advanced calculus and blogging about it) — this will be a podcast to keep your ear on. Subscribe to it!

That handsome young studmuffin at the other end of the bar may not look as good as a reliable, if boring, man once you’re taking a daily dose of hormones. That’s one of the conclusions drawn by a team of scientists, who’ve previously shown that where women are in their monthly cycle affects what kinds of men they select as potential mates from a series of photographs, after they took their work out of the lab and interviewed more than 2500 women to see what effect the pill has on their real-life decisions.

In lab studies, women who are in fertile stages of their cycle are more likely to go for men who look healthy, self-confident, and masculine, which tend to be markers for good genes, but also for infidelity. The pill mimics pregnancy, though, when the die has already been cast and being a good provider is more attractive than sexy. In the lab, women on the pill do indeed select men who look like they will be more reliable and steady.

But outside the lab, would those patterns hold? After collecting data on their subjects’ sexual satisfaction and general satisfaction with their partners (each of them had had children with a partner, and in many cases was still with him), the team found that women who had met their partners while on the pill reported less sexual satisfaction but greater general satisfaction than women who had been off the pill. In other words, their partners were good fathers and good providers, but not necessarily on fire between the sheets. The trends seen in the lab seem to hold true (although we hasten to point out that the pill can sometimes kill women’s sex drive—an alternate explanation for why sexual satisfaction might be lower).

What happens when these women go off the pill, though? Do their marriages hold up, buoyed by the presence of children and their husband’s attributes as a father, or does a renewed attraction to the studmuffin make things shakier? That’s a topic for another study, looking more explicitly at the ends of relationships and tracking pill use throughout.

Reference: S. Craig Roberts, et al. Relationship satisfaction and outcome in women who meet their partner while using oral contraception. Published online before print October 12, 2011, doi: 10.1098/rspb.2011.1647 Proc. R. Soc. B

Image courtesy of istolethetv / flickr

Every year, thousands of people die because of typos in their genes. There’s a long list of debilitating or fatal genetic diseases that are caused by a single incorrect DNA letter among the three billion in our genome. It’s the equivalent of pulping an entire encyclopaedia on the basis of a single typo. But hope is at hand. We are fast approaching the point when we can proofread these errors out of our genes.

Kosuke Yusa  and Tamir Rashid have taken the latest step towards this goal, by developing a more efficient and less risky way of correcting genetic errors. They took cells from patients with a genetic liver disease, edited the gene responsible, and grew corrected liver cells that successfully treated mice with the same disease.

The disease in question is called alpha 1-antitrypsin deficiency (or alpha-1 for short). It affects 1 in every 2,000 Europeans and is caused by a single typo in the A1AT gene. The error stops people from making enough of the A1AT protein. The little they do make builds up in their liver, overloading it and leading to cirrhosis. At the moment, the only treatment is a liver transplant, and donors are hard to come by.

Yusa and Rashid fixed this problem in three steps: they took skin cells from alpha-1 patients with two bad copies of the A1AT gene; reprogrammed them into stem cells; fixed the error in both copies of the broken gene; and used the corrected stem cells to produce liver cells. This is the first time that anyone has corrected a faulty gene in stem cells derived from a human patient.

The first step relies on methods that were first developed in 2006. In August of that year, Shinya Yamanaka from Kyoto University found a way of reprogramming adult cells so they could create any type of tissue in the body. He could imbue adult cells, which are normally fixed in specific roles, with the limitless potential of stem cells. Since then, research on these “induced pluripotent stem cells” or iPSCs, has raced along at blistering speed. Scientists quickly realised that they could use iPSCs to create an unlimited supply of tissues and organs, tailored to a person’s own genome. They could even fix errors in the reprogrammed cells to create working tissues in people who were suffering from genetic disorders.

A few groups have successfully done this in mice. In 2007, Rudolf Jaenisch used the iPSCs to cure mice of a genetic disorder called sickle cell anaemia, caused by deformed blood cells. Jaenisch made iPSCs from skin cells in the rodents’ tails, corrected the faulty gene that was behind their disease, and injected the cells back into the mice. Just four weeks later, the mice started producing normal blood cells. In 2009, Yupo Ma used the same methods to treat a second genetic disease called haemophilia A, again in mice.

But there are two big problems with these methods. First, they’re not very efficient. If you start off with a large batch of iPSCs with the same faulty gene, you only ever correct a small proportion of them. To single them out, scientists rig the editing process so the corrected cells also gain a marker – say, a gene that makes them resistant to a particular antibiotic. That makes them easy to identify and isolate. Once this is done, the marker can be cut out. That leads to the second problem: the markers tend to leave small bits of DNA behind. In fixing one error, you could introduce several more. At worst, the DNA remnants could disrupt important genes and cause cancers.

Yusa and Rashid solved both of these problems. First, they designed a scissor-like protein called a ‘zinc finger nuclease’ to specifically cut the A1AT gene at its incorrect letter. By precisely targeting the typo, the team could efficiently replace it with the right letter.

Second, they created a marker that can be seamlessly removed. They relied on a jumping gene called piggyBac, which can cut itself out of its surrounding DNA and paste itself back into a different spot. It does so flawlessly; once it jumps out of a piece of DNA, you’d never be able to tell that it was once there. By loading their marker gene into piggyBac, Yusa and Rashid could yank it out once they had identified the corrected cells, without leaving any traces behind or disrupting any genes.

The duo used their corrected iPSCs to grow new liver cells, which produced normal working versions of the A1AT protein. They transplanted these cells into mice with the same faulty gene. Two weeks later, the cells had colonised the rodents’ livers, they were behaving normally, and they hadn’t produced any tumours.

That’s reassuring because even with their new technique, the results weren’t entirely faultless. Yusa and Rashid found that the liver cells had gained 29 new mutations since their days as skin cells. Most of these happened when they were reprogrammed back into stem cells. One was caused by the zinc finger nuclease, and three were due to piggyBac. This isn’t necessarily a problem; cells naturally acquire fresh mutations over time and most are of no consequence. Still, the mutations add a note of caution to an otherwise optimistic study.

The next step will obviously be to test the final transplant stage with human patients. The team want to take things slowly, testing the technique in degrees to make sure that it’s safe for patients. This will probably take several years but they are keen that the hype doesn’t outrun the pace of their work.

For people with alpha 1-antitrypsin deficiency, the technique could solve the shortage of liver transplants. You don’t need a donor when you can just grow a new liver from your own corrected stem cells. Even better, that liver would be genetically identical to the rest of your body, so you wouldn’t have to worry about rejection or immune problems.

The liver is a good place to start when trying to prove that this technique can work, because it regenerates very well naturally. Other organs might be trickier; new neurons, for example, would need to connect with the existing network. Even so, Yusa and Rashid’s study has implications for other genetic diseases. The same techniques could be used to correct other genetic faults – using the zinc finger nuclease to make things more efficient, and piggyBac to avoid disrupting the surrounding genes.

Reference: Yusa, Rashid, Marchand, Varela, Liu, Paschon, Miranda, Ordo, Hannan, Rouhani, Darche, Alexander, Marciniak, Fusaki, Hasegawa, Holmes, di Santo, Lomas, Bradley & Vallier. 2011. Targeted gene correction of a1-antitrypsin deficiency in induced pluripotent stem cells. Nature http://dx.doi.org/10.1038/nature10424

Image by Sirsnapsalot

More on regenerative medicine:

• Gene therapy saves patient from lifetime of blood transfusions
• An entire flatworm regenerated from a single adult cell
• Research into reprogrammed stem cells: an interactive timeline
• Lungs rebuilt in lab and transplanted into rats

Just a quick reminder: I’m participating in a blogger’s challenge with Donors Choose to raise money to get science supplies for classrooms in need. I have added a link in the sidebar of the blog (just below the picture of me) so that you can see how much has been raised, and which also provides a link to the donation page.

If you can’t donate, that’s fine, but if you could, please help spread the word through the social networks; Twitter, Facebook, Google+, whatever you can. This is a great way to get people to contribute directly to kids who need to learn about the joy and wonder of exploring the Universe. Thanks!

As the 2012 presidential race ramps up, campaigns are courting voters not only at the traditional county fairs and town hall meetings, but online—and generating, in the process, an enormous amount of data about who potential voters are and what they want. At CNN.com, Micah Sifry—an expert on the intersection of technology and politics—delves in the Obama team’s extensive efforts to mine and manage the data in a way that could help them better interact with voters and home in on important issues. He writes:

Inside the Obama operation, his staff members are using a powerful social networking tool called NationalField, which enables everyone to share what they are working on. Modeled on Facebook, the tool connects all levels of staff to the information they are gathering as they work on tasks like signing up volunteers, knocking on doors, identifying likely voters and dealing with problems. Managers can set goals for field organizers — number of calls made, number of doors knocked—and see, in real time, how people are doing against all kinds of metrics.

No Republican candidates, however, seem to have similar systems in place to help them manage and use this data. Republican technology consultant Mark Avila spoke to Sifry of the Republican presidential hopefuls:

“They have to stop seeing a website as a piece of direct mail that people will receive,” he said. “They have to see a website as the equivalent of a campaign office in Iowa, one that is open 24/7.” And campaigns need to know how to take quick and well-targeted action to respond to every expression of interest they may get online, he argues, because voter interest in politicians is fickle. Simply sending a generic e-mail reply isn’t enough.

“If you can make that initial response a phone call from someone in their town or a neighbor, asking them to come to a county fair tomorrow, that’s much more powerful.”

Read the rest at CNN.

Photo courtesy of the White House / Flickr

In Bar-Yam’s model, areas where different language groups overlap have a high likelihood of ethnic violence (E). Once administrative boundaries are included, the risk of violence drops–except for a northwestern region, where ethnic violence has in fact occurred (F).

Ethnic violence is one of the bloodiest and most virulent kinds of conflict. Pinpointing areas where it’s likely to erupt and sussing out why some areas have avoided it are intensely interesting issues to geographers, and Yaneer Bar-Yam of the New England Complex Systems Institute made headlines four years ago with a model indicating that how messy the borders are between ethnic groups may be a good predictor of violence. Now, after using it to predict where violence was likely to occur in India and the former Yugoslavia, both areas known for their ethnic turbulence, he’s posted a paper on the ArXiv that applies his analysis to Switzerland, a enviably peaceful country that nevertheless has four national languages and large, devout populations of both Protestants and Catholics. How do the Swiss do it, he asks?

His team’s answer, basically, is geographic and administrative isolation. Switzerland is divided up into cantons—states that each run almost autonomously—that are fairly homogenous in terms of language and religion, and the country’s mountains and lakes provide geographic barriers between regions that might clash. Looking at data from the 2000 census, they found that the one area where the model predicted a reasonable possibility of violence, based on the mixing pattern of languages and religions, was the region northwest of Bern where in fact there was significant violence in the 1970s. The Jura separatist movement—a group dedicated to creating a French-speaking canton from part of the predominantly German-speaking canton of Bern—resorted to arson around that time, and in 1979, Jura was recognized as its own canton. (But the borders were drawn along the lines of religion, rather than language, and the violence did not completely subside; at the moment, the government is considering lumping the French Protestants of Bern in with the French Catholics of Jura to alleviate the problem.) Trying to get everyone in area to feel brotherly to one another may not be an effective way to manage violence, Bar-Yam and colleagues write. For assimilation to work, no group should be so large as to have an independent identity or public spaces that they identify with, they say, and in the absence of that, partition may be a better option.

While this work is certainly food for thought, it raises a number of questions. Partition along religious lines did not work well at all for India and Pakistan. Bar-Yam and colleagues do not address what specific characteristics—in terms of previous conflict, general climate, and political response—are required for new borders to quench violence. One might make the argument that the long and bloody conflict prior to Partition could be in play in the India-Pakistan example, but it’s clearly more complicated than that: Before the establishment of the modern cantons, Switzerland, that bucolic icon of peace, had 200 years of intermittent religious conflict.

Image courtesy of Rutherford, et al.

Here’s a blast from the somewhat-recent past: a set of five lectures I gave at CERN in 2005. It looks like the quality of the recording is pretty good. The first lecture was an overview at a colloquium level; i.e. meant for physicists, but not necessarily with any knowledge of cosmology. The next four are blackboard talks with a greater focus; they try to bring people up to speed on the basic tools you need to think about modern early-universe cosmology.

Obviously I’m not going to watch all five hours of these, so I’ll just have to hope that I’m relatively coherent throughout. (I do remember being a bit jet-lagged.) But I do notice that, while it was only a few years ago, I do appear relatively young and enthusiastic. Ah, the ravages of Time…

Lecture One: Introduction to Cosmology

Lecture Two: Dark Matter

Lecture Three: Dark Energy

Lecture Four: Thermodynamics and the Early Universe

Lecture Five: Inflation and Beyond

This is an updated version of an old piece, edited to include new information. Science progresses by adding new data to an ever-growing picture. Why should science writing be different?

The road of East Smithfield runs through east London and carries a deep legacy of death. Two cemeteries, established in the area in the 14^th century, contain round 2,500 of bodies, piled five deep. These remains belong to people killed by the Black Death, an epidemic that killed between 30 and 50 percent of Europe in just five years. It was one of the biggest disasters in human history and seven centuries on, its victims are still telling its story.

In the latest chapters, Verena Schuenemann from the University of Tubingen and Kirsten Bos from McMaster University have used samples from East Smithfield to reconstruct the full genome of the bacterium behind the Black Death. This species – Yersinia pestis – still causes plague today, and the modern strains are surprisingly similar to the ancient one.

Compared to the strain that acts as a reference for modern plague, the ancient genome differs by only 97 DNA ‘letters’ out of around 4.6 million. Y.pestis may not be the same bacterium that butchered medieval Europe 660 years ago, but it’s not far off. Indeed, Schuenemann and Bos found that all of the strains that infect humans today descended from one that circulated during the Black Death. Even now, people are still succumbing to a dynasty of disease that began in the Dark Ages.

The Black Death is supposedly the second of a trilogy of plague pandemics. It came after the Plague of Justinian in the sixth to eighth centuries, and preceded modern plague, which infects some 2,000 people a year. But some scientists and historians saw features in the Black Death that separates it from other plague pandemics – it spread too quickly, killed too often, recurred too slowly, appeared in different seasons, caused symptoms in different parts of the body, and so on.

These differences have fuelled  many alternative theories for the Black Death, which push Y.pestis out of the picture. Was it caused by an Ebola-like virus? An outbreak of anthrax? Some as-yet-unidentified infection that has since gone extinct? In 2000, Didier Raoult tried to solve the debate by sequencing DNA from the teeth of three Black Death victims, exhumed from a French grave. He found Y.pestis DNA. “We believe that we can end the controversy,” he wrote. “Medieval Black Death was plague.”

Raoult was half-wrong. The controversy did not end. Some people argued that it’s not clear if the remains came from Black Death victims at all. Meanwhile, Alan Cooper analysed teeth from 66 skeletons taken from so-called “plague pits”, including the one in East Smithfield. He found no trace of Y.pestis. Other teams did their own analyses, and things went back and forth with a panto-like tempo. Oh yes, Y.pestis was there. Oh no it wasn’t. Oh yes it was.

In 2010, Stephanie Haensch served up some of the strongest evidence that Y.pestis caused the Black Death, using DNA extracted from a variety of European burial sites. Schuenemann and Bos bolstered her conclusion by taking DNA from bodies that had been previously exhumed from East Smithfield, and stored in the Museum of London. “We sifted through every single intact skeleton and every intact tooth in the collection,” says Bos. They extracted DNA from 99 bones and teeth and found Y.pestis in 20 of them.

Schuenemann and Bos took great care to ensure that their sequences hadn’t been contaminated by modern bacteria. Aside from the usual precautions, they did all of her work at a facility that had never touched a Y.pestis sample, they had the results independently confirmed in a different lab, and they found traces of DNA damage that are characteristic of ancient sequences. They also failed to find any Y.pestis DNA in samples treated in exactly the same way, taken from a medieval cemetery that preceded the Black Death. Finally, it’s clear that the people exhumed from East Smithfield did indeed die from the Black Death – it’s one of the few places around the world that has been “definitively and uniquely” linked to that pandemic.

Even though they had its DNA, deciphering the ancient bacterium’s genome was difficult. The DNA was so heavily fractured that Schuenemann and Bos only managed to extract enough from four of their teeth. They lined up the fragments against a modern plague genome, and looked for overlaps between the remaining stragglers. In the draft that they’ve published, every stretch of DNA has been checked an average of 28 times.

By comparing this ancient genome with 17 modern ones, and those of other related bacteria, Scheuenemann and Bos created a family tree of plague that reveals the history of the disease. They showed that the last common ancestor of all modern plagues, lived between 1282 and 1343 before it swept through Europe, diversifying as it went. The East Smithfield strain was very close to that ancestral strain, differing by only two DNA letters.

This raises some questions about the plague of Justinian. The team think that it was either the work of an entirely different microbe, or it was caused by a strain of Y.pestis that is no longer around and likely left no descendants behind. It was the supposed second pandemic – the Black Death – that truly introduced Y.pestis to the world. This global tour seeded the strains that exist today.

By the time it hit East Smithfield, the plague was already changing. Schuenemann and Bos found that one of their four teeth harboured a slightly different version of Y.pestis, which was three DNA letters closer to modern strains than the other ancient ones. Even in the middle of the pandemic, the bacterium was mutating.

In the intervening centuries, Y.pestis has changed but not by much. None of the few differences between the ancient and modern genomes appear in genes that affect how good the bacterium is at causing diseases. None of them can obviously explain why the Black Death was so much more virulent than modern plague. “There’s no particular smoking gun,” says Hendrik Poinar, who was one of the study’s leaders.

That’s somewhat anticlimactic. In August, Poinar told me: “We need to know what changes in the ancient [bacterium] might have accounted for its tremendous virulence… There is really no way to know anything about the biology of the pathogen, until the entire genome is sequenced.” Now that the full genome is out, it seems to offer precious few clues.

Instead, the team thinks that a constellation of other factors might have made the Black Death such a potent pandemic. At the time, medieval Europe went through a drastic change in climate, becoming colder and wetter. Black rat numbers shot up, crops suffered and people went hungry. “It’s hard to believe that these people living in 1348 London weren’t being infected by various viruses,” says Poinar. “So you probably had an immune compromised population living in very stressful conditions, and they were hit by Y.pestis, maybe for the first time.” They were both physically and culturally unprepared. Their immune systems were naive, they didn’t know what the disease was, and they didn’t know how to treat or prevent it.

In later centuries, it was a different story. Medical treatments helped to cope with the symptoms and affected people were quickly quarantined. Today, we have antibiotics that help to treat plague, and these would be effective against the Black Death strain. We have evolved too. People who were most susceptible to plague were killed, which probably left the most resistant survivors behind. Next, Poinar wants to look at the DNA of people buried in pre-plague and post-plague cemeteries to see if the Black Death had altered our own genome.

Sequencing the Black Death genome may not tell us about why it was so deadly, but it still reveals how the bacterium evolved. Now, Schuenemann and Bos can look at how Y.pestis transformed from a bacterium that infects rodents to one that kills humans and how it evolved over time. That knowledge could be very important, especially since plague is rebounding as a “re-emerging” disease.

The Black Death strain is the second historical pathogen whose genome has been sequenced and certainly the oldest (the first was the 1918 pandemic flu). There are many others to look at, including the Justinian plague strain, and historical versions of tuberculosis, syphilis and cholera.

In the meantime, the East Smithfield bodies have told their story and Bos and Schuenemann are letting them rest. They were very careful with the teeth that they yanked DNA from, and they are now returning these samples to the Museum of London. Having yielded their secrets, they’ll be stuck back into their old skeletons.

Reference: Bos, Schuenemann, Golding, Burbano, Waglechner, Coombes, McPhee, DeWitte, Meyer, Schmedes, Wood, Earn, Herring, Bauer, Poinar & Kruase. 2011. A draft genome of Yersinia pestis from victims of the Black Death. Nature http://dx.doi.org/10.1038/nature10549

Schuenemann, Bos, deWitte, Schmedes, Jamieson, Mittnik, Forrest, Coombes, Wood, Earn, White, Krause & Poinar. 2011. Targeted enrichment of ancient pathogens yielding the pPCP1 plasmid of Yersinia pestis from victims of the Black Death. PNAS http://dx.doi.org/10.1073/pnas.1105107108

PS Oddly, the team’s new paper, where they publish the full Black Death genome, somewhat refutes their first one, where they had only sequenced fragments. Previously, they identified two mutations in the ancient DNA that weren’t seen in any other strain. But those two mutations aren’t there in the full genome, and it now seems that they were a mistake. Ancient DNA can be chemically damaged so that Cs change into Ts. That’s probably what happened in the previous study. Schuenemann and Bos are more confident that their new sequences are correct. They treated their samples with a method that repairs the C-to-T changes, and they went over every bit of DNA 30 times.

Image: Skeletons from the Museum of London;

Larry Moran thinks that I had to ask my parents and siblings for permission before publishing my genotype. Interestingly, most of his readers seems to disagree with Larry on this, so I won’t offer my own response in any detail. They’re handling it well enough. I would like to add though that obviously this isn’t a either/or proposition. If my family had a history of a particular genetic disease which was well characterized in terms of causative alleles I might not have published my genotype. As it is, we don’t. So I didn’t see much of a downside. I would also add that in my case It wasn’t possible to have genuine consent in the first place. My mother isn’t much into science, and we don’t share a common first language. There’s really no way that I could have gotten substantive consent, insofar as my mother understood what I was doing.

More broadly though I think it is useful to broach this question and think about it. People do have social responsibilities by and large, and we’re embedded in a broader fabric. This isn’t true in all cases, some people have such horrible relationships with their families (e.g., victims of abuse) that it’s obviously ridiculous to wonder if they should ask their family for consent.

We’ve sent space probes to every planet in our solar system (and if you’re a die-hard Pluto fan, you only have to wait 4 more years). And yet there is still much to see, much to explore. Not every world gives up its secrets easily, and perhaps none has been so difficult to probe than Titan, Saturn’s largest moon. Bigger than Mercury, second only to Jupiter’s Ganymede, Titan has an atmosphere of nitrogen so thick it has twice the Earth’s air pressure at its surface.

That thick, hazy atmosphere is impenetrable by optical light… but infrared light can pierce that veil, and the Cassini space probe is well-equipped with detectors that can see in that part of that spectrum. And after 7 years, and 78 fly-by passes of the huge moon, there are enough images for scientists to make this amazing global map:

Pretty awesome. And making this animation was a huge effort. First, not all of the passes were at the same distance, so scientists had to resize the images to match the scale. Cassini passed at different times of day for the local regions, so the sunlight angle changed, making illumination and shadowing different. The atmosphere of Titan is dynamic, changing with time, so again compensations must be made. It’s painstaking work, but the results are truly incredible:

In this false-color map, what’s shown as blue is actually light at a wavelength of 1.27 microns — very roughly twice the wavelength the human eye can detect. Green is 2 microns, and red is 5 microns, well out into the infrared. When the final images are combined, what show up as brown regions near the equator are actually vast dune fields, grains of frozen hydrocarbons rolling across the plains in the relentless Titanian winds. White areas are elevated terrain. Near the north pole, only barely visible, are smudges on the map that have been shown to be lakes — literally, giant lakes of liquid methane!

So Titan has air, lakes, and weather. Sound familiar? It’s not exactly Earth-like, since the temperature there is roughly -180°C (-300°F), but the similarities are compelling. And Titan is loaded with organic compounds like methane, ethane, and more. A complex chemistry is certainly possible there, but complex enough to have formed life? No one knows. Just a few years ago I don’t think anyone would’ve taken the possibility seriously, but now… well, I wouldn’t rule it out.

Remember, these maps only show global features, and even though Cassini dropped the Huygens probe onto the surface, it saw a tiny fraction of what there is to see on this moon, which boasts over 80 million square kilometers of territory. That’s a lot of land. What else is there to find there?

[UPDATE: Just to be clear, this is the first global multicolor map of Titan; a map in single color was done in 2009.]

Credit: NASA/JPL/University of Arizona/CNRS/LPGNantes

Josephine Schuppang of Technical University in Berlin writes, I was pointed to your blog when I talked to a friend about my newest tattoo. He told me that you are collecting scientific tattoos. I didn’t even know there were other people who did that sort of thing. You bet my tattoo artist looked strangely at [...]