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There's a Hole in the Bottom of the Sea

"There's! A! Flea, on the fly, on the wart, on the frog, on the bump, on the log--" Does anyone else remember this song? Because it has been going through my head ever since I started reading about the human virome. That's the viruses that live inside the bacteria that live inside us.

First there was the genome--all the DNA in a human--which we've now got a pretty good handle on. It turned out that our smallish number of genes can be shuffled into a larger number of RNA "transcripts,"  so there's also the transcriptome. Those transcripts are used to make the proteins in our body, naturally known as the proteome. The microbiome is all of the microorganisms that live inside humans. (Don't look now, but there are 10 times more of their cells than yours in your body.) And the virome goes a step more microscopic, to the viruses.

The bacteria inside us have been the subject of a lot of interesting research lately. They occupy us as paying tenants, helping to digest our food and performing other mysterious functions that seem to maintain our good health. Existing around and in those bacteria are viruses that vastly outnumber even the bacterial cells.

Some scientists are starting to explore the role these viruses play in our bodies. At Washington University in St. Louis, Jeffrey Gordon and his colleagues studied the viruses inhabiting four sets of adult identical twins and their mothers. (They did this by sequencing the viral genes in their stool samples.) Previous studies had shown that twins and their mothers have more similar bacterial populations than unrelated people do. Surprisingly, though, there was no such connection between the viral populations--people have unique viromes, regardless of how related they are.

But the viral populations seemed to be stable. In three samples taken over the course of a year, the subjects' viromes were consistent. So the differences between people aren't due to a constant turnover in the types of viruses they harbor.

Furthermore, Gordon found evidence that the bacteria and the viruses that attack them (called phages) were coexisting relatively peacefully, and not engaging in the turf war that might be expected.

So what are they doing in there? Are they helping us? Hurting? Neither or both? Gordon suggests that studies of the human microbiome should include the virome, so we can find out.

One interesting preliminary result has come from another set of researchers at Washington University who are studying viruses in babies. Looking at the viral genes in babies' nasal samples, they compared healthy babies to babies with unexplained fevers. They say they found 10 times more viruses in the feverish babies. It's not clear whether the viruses are to blame for the fevers or something more complicated is going on. But if doctors learn that the virome is to blame in these cases, they could avoid prescribing unnecessary antibiotics (since antibiotics only treat bacterial infections).

It's good to avoid unnecessary antibiotic use, of course, because it encourages bacteria to develop resistance to those drugs. That brings up another point about the virome: Phages, the viruses that prey on bacteria, sometimes drag bacterial genes between their victims. A gene for antibiotic resistance, for example, could be spread among a population of bacteria in your body by the viruses there.

More alarming and interesting relationships will, no doubt, emerge as scientists continue to learn about the microscopic menageries inside us. I just hope they don't find any more "omes." Really, it's enough already.

A Cloud and a Silver Lining, Part II

Last week, things were looking pretty bad at the Fukushima Daiichi nuclear power plant in Japan. (See the first installment of "A Cloud and a Silver Lining" here.) Since then, helicopters and firehoses have intervened, spinach and drinking water have caused concerns, and things are looking...still pretty bad.

Keeping the fuel in the reactors cool, as well as the used fuel rods that are stored in pools of water, is crucial to preventing radiation from leaking out. Heat from the fuel rods makes water boil off of them, so it has to be constantly replaced. Helicopters were used last week to dump water into the spent fuel pools from above, while firehoses sprayed water onto the reactors. Early this week, workers were finally able to string power cables to the plant's six reactors, restoring electricity. That meant the cooling systems (at least, their non-damaged components) could be turned back on, though workers would still have to fight  to clean up the radioactive material and stop the leaks.

Then radioactive iodine showed up in Tokyo's tap water. The levels weren't dangerous for adults, but the government urged parents not to let babies drink any tap water--since their thyroid glands are still developing, they're more liable to absorb the cancer-causing isotope. Radioactive iodine and cesium have also turned up in milk and vegetables (such as spinach) around Fukushima. Japan has banned the sale of these products, and the United States has stopped importing dairy and produce from the region. Luckily, the radioactive iodine has a half-life of just 8 days, so it won't stick around for very long--once it stops coming out of the nuclear plant, that is. But the radioactive cesium has a half-life of 30 years. This means its presence in farmlands could become a very long-term problem.

Differing evacuation recommendations from the Japanese and American governments have caused confusion and tension. The Japanese government ordered a total evacuation within 20 kilometers (12 miles) of the plant, and told people between 20 and 30 kilometers away to stay indoors. Meanwhile, the U.S. government urged its citizens in Japan to stay 50 miles away from the plant. The Nuclear Regulatory Commission's reasons for the 50-mile recommendation were somewhat unclear, since the radiation reaching that far from the plant is, so far, negligible. But the NRC may have been betting against Japan's ability to subdue the growing nuclear crisis.

Today, the Japanese government seemed to similarly lose confidence, widening the evacuation zone to 30 kilometers (19 miles). Those residents aren't being ordered to leave--though, after staying indoors all this time, they might be happy to. A new concern is that one building's reactor vessel may be leaking radioactive material. Two workers suffered radiation burns from water that sloshed into their boots near the reactor. An anonymous nuclear executive told the New York Times that the vessel has a "definite crack."


So where's the silver lining? Radiation levels in the Tokyo tap water dropped, making it safe for infants again. And though the Japanese government has been less than transparent about the situation at Fukushima Daiichi, people have begun gathering and distributing information on their own. Several sites are using crowd-sourced data to create maps of the radiation in Japan. This site uses Google Earth to map radiation levels, which puts the disaster into beautiful perspective even as it continues to unfold.


Wrinkly Dog Syndrome


To say that the Shar-pei is a wrinkly dog is putting it mildly. The ones that have been bred in China for hundreds of years are identifiable by a furrowed brow that makes them look permanently concerned (D). The Shar-Pei dogs bred in the West, though (A-C), have been turned into baggy overgrown puppies that can barely see you from behind their folded-up faces.

Like other purebreds, the Shar-Pei has health problems. Some of them are symptoms of its desired traits (such as a susceptibility to infections inside its skin folds), while others are genetic accidents that come from generations of inbreeding and artificial selection. A condition called Familial Shar-Pei Fever (FSF) is one of those genetic disorders. But a new study has shown that, rather than being a genetic fluke, FSF comes from the very same mutation that causes the dogs' wrinkliness. The disease has been bred into them along with their cute, scrunchy faces.

Researchers in Sweden (one of whom is named, improbably, Puppo) compared the DNA of a group of Shar-Pei dogs to dogs of other breeds. They found a pronounced difference on chromosome 13, in the genetic region that makes a gooey molecule called hyaluronic acid (HA). This was no great surprise: the Shar-Pei's thick and wrinkled hide is known to be caused by a huge buildup of HA in the skin.

The surprise came when the researchers divided up the Shar-Pei group into those affected and unaffected by FSF. The disorder causes frequent fevers and inflammation. Scanning the genome for a region associated with the disorder, the researchers found themselves right back at chromosome 13. The wrinkly-skin mutation is a duplication--a certain chunk of DNA copied one or more times. The dogs had varying numbers of duplications, like a stutter in this genetic region. And the scientists saw that the dogs with the most copies were the most likely to have the fever disorder.

So the very trait that breeders have valued in the Shar-Pei is what makes it ill. The problem may arise from broken fragments of HA molecules, which might encourage inflammation. The authors speculate that excess HA might be responsible for even more of the Shar-Pei's health problems, such as skin allergies, tumors, and kidney damage.

But the good news is that the wrinkly dogs might be able to help humans. Some people suffer from inherited fever syndromes that are similar to FSF. A few genetic links have been found, but about 60% of these cases have no known cause. Future research might find a link between hyaluronic acid and chronic fever disorders in humans, leading to new treatment possibilities. Of course, the best treatment for the Shar-Pei would be to stop breeding it. But as long as people keep demanding squishy-looking pets, that seems unlikely.


Image: PLoS Genetics/doi:10.1371/journal.pgen.1001332.g001

The Japanese Blues

You've seen those posters in the subway: "If You See Something, Say Something." It sounds like a reasonable summation of how language works. First we see something, then we connect it to the right word or words in our mind, and then we are able to say something about it. But can it also work backward?

Some scientists think that how we talk about a thing can influence how we perceive it. An easy way to test this is with colors, and studies in the past have shown that people are more likely to see two colors as similar if their language groups those colors together under one name. If there are more names for colors, people may be better able to tell the difference between them.

In Japanese, there are two words for blue: ao is darker blue and mizuiro is lighter blue. (These are just the common, one-name terms; obviously any English speaker with a Crayola box could come up with a dozen kinds of blue. But you're unlikely to categorize something as "cornflower" or "cerulean.")

Linguist Panos Athanasopoulos and his colleagues wanted to know if Japanese-English bilinguals would  perceive blues more like English speakers or more like Japanese speakers. Would they understand blue as two colors, or one? To test this, they gathered 27 bilinguals, all native Japanese speakers who were college or graduate students in the UK. They also recruited 27 monolingual subjects; half were English speakers, and the other half were Japanese students who had just arrived in the UK to begin studying English.

The subjects were shown pairs of blue squares with varying hues and asked how similar the two colors were (on a scale of 1 to 10). There were 10 different blues used in there experiment, and all of them had been consistently described as ao or mizuiro by Japanese speakers in a previous experiment. The researchers expected that in this experiment, Japanese speakers would see the pairs as less similar if one was ao and the other was mizuiro.

They found that English speakers, as expected, categorized their colors independently of whether they were ao or mizuiro. (So even though the two categories exist in Japanese, they're not inherent to how we see color.) Japanese monolinguals described dissimilar pairs of blues as even less similar if one was ao and the other was mizuiro. And the bilinguals were sort of in between: they were only slightly influenced by whether a color was ao or mizuiro. Learning English had apparently blurred the categories together in their perception. Analyzing their data further, the researchers found that among the bilinguals, those who had more experience in English increasingly ignored the ao/mizuiro distinction.

The researchers made sure gender wasn't affecting their results. In this country, men are notorious for not being able to distinguish between colors. Even if it's true, this study reminds us that a difference in perception doesn't necessarily come down to how well your eyes work. Maybe boys in America are taught not to enjoy all the cornflowers and ceruleans and forget-me-not blues, and as a result never learn to distinguish them.

"Language is the mechanism that assists the influence of culture on cognition," the authors write. That is, our vocabulary influences how we perceive the world, and that vocabulary comes from the culture we live in. In the weeks and years to come, we'll see how the Japanese translate their new blues into words. Not only can we not comprehend the loss the country experienced in the earthquake and tsunami, or the danger they feel from the ongoing nuclear crisis--but we wouldn't even experience it the same way if we were there.

A Cloud and a Silver Lining

For the past few days, the only science news I've been thinking about is happening in Japan.

There have been a few pleasant diversions: elephants that understand teamwork; whales that seem to address each other by name; office workers who boost their attention spans using houseplants. But the nuclear disaster seems more important to talk about right now.

In case you've missed it, the one-two punch of unprecedented earthquake and massive tsunami overwhelmed Japan's Fukushima Daiichi nuclear plant, which has six nuclear reactors. Though the reactors automatically shut down in the earthquake, a series of explosions, fires, and leaks has kept workers racing to prevent a large-scale release of radiation. To compensate for failed cooling systems and prevent reactors from melting down, workers have been pumping in seawater, which constantly boils away. Also of concern are pools at the top of each reactor that hold used-up fuel rods to cool for many years. If these pools boil dry, the old fuel could catch fire and release radioactive material.

750 workers were evacuated from the plant on Tuesday because of the high levels of radiation there. A skeleton crew of just 50 workers stayed behind to try to prevent a larger disaster. (In order to keep the skeleton crew at the plant, the Japanese government raised the legal limit on radiation exposure for workers.) That number may have now been increased to 100 people.

Accurate information has been hard to come by. Last night, a Japanese official giving a press conference announced (via a translation that seemed pretty approximate) that all workers had been evacuated from the plant. This seemed to imply, grimly, that they were giving up on containing the radiation--until the Times reported that the small crew of workers was, in fact, still at the plant trying to cool things down.

There is some good news. If large amounts of radiation are released, the Japanese government is prepared with potassium iodide pills. These pills flood the body with iodine so the thyroid gland doesn't absorb any radioactive iodine, leading to thyroid cancer. (An epidemic of thyroid cancer was the legacy of Chernobyl.)

Additionally, radiation is expected to blow east. That means this developing disaster has a greater buffer zone--the entire Pacific--than it would probably anywhere else in the world.

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For answers to all kinds of questions on this subject as they arise, check out ScienceInsider or the New York Times.

Trust Your Gut

At Washington University in St. Louis, researchers have found that humans' ability to survive starvation may depend on the kinds of bacteria living in their guts. They deduced this by feeding poop and peanut butter to mice.

How about I back up a little.

If you haven't heard, the hot new field in biology is the "microbiome." There's even a Human Microbiome Project, started in 2008. It's reminiscent of the Human Genome Project, which pushed through the 1990s and early 2000s to complete a sequence of the human genome. But the microbiome isn't made of human DNA, or human anything. It's the collection of bacteria and other microorganisms that live inside us. And it's starting to seem pretty important.

Your microbiome is not an everyday cold or patch of infection. It's the Alamo. For every single cell in your body, there are 10 microbial cells. Yes, in your body. The only reason you look like a person and not a big oozing blob is that your cells are way bigger. Most of these microbes live in a thick layer in your intestines, where they help you digest certain foods but otherwise stay out of your business. In addition to the gut, your microbial companions (also called, rather romantically, your "flora") live in your various orifices and all over your skin.

Microbes first colonize humans at the moment of our birth. But our microbial populations can change over time: we eat things, touch things, get sick, take antibiotics. Scientists are just beginning to understand the relationship between our gut flora and our overall health. It's not a trivial relationship; we've evolved with this population as a part of our bodies.

The researchers in St. Louis are studying the role of gut bacteria in malnutrition. Specifically, they're looking at twins growing up near-starving in Malawi. Even though they have the same genes and eat the same food (what there is of it, anyway), the twins sometimes respond differently. One twin may develop kwashiorkor, the bloated-belly form of malnutrition that we see in photos from impoverished countries, while the other twin doesn't.

As ScienceNOW reports, the scientists wondered if different gut bacteria might be responsible for different responses to malnutrition. To test their theory, they took stool samples from a pair of twins like those described above. They fed the two stool samples to two groups of mice that had been carefully kept sterile since birth, in order to colonize the mice with the children's gut bacteria. Then they alternated between feeding the mice a typical Malawian diet (mostly corn flour) and a food used to treat malnutrition (which includes peanut butter).

The mice with the healthy twin's bacteria maintained a more stable weight, and a more stable population of gut flora, than the mice with the kwashiorkor twin's bacteria. Though this was just a pilot study, it suggests that gut bacteria may be crucial to humans' ability to survive starvation.

More applicable to most of us in the Western world was a 2009 study out of the same Washington University lab. Looking at gut microbes from obese and non-obese twins, the scientists found that the obese people had fewer types of bacteria in their guts. They also found that mothers and their children share a lot of their gut flora, regardless of whether the children are identical twins. This implies that our microbial makeup has much more to do with our environment than our genes.

In the future, doctors may use this kind of information to treat patients with microbial therapy--instead of drugs, why not put the right balance of bacteria into your body and let them do the work? Some doctors are already using so-called fecal transplants, which are exactly what they sound like. Is it gross? Yes. But pretty soon, we may have to get over it and admit that our microbes are looking out for us.

Mind-Control Fungi: You Can't Look Away

I wish I could tell you this is the rare Brazilian dead-eyed reindeer ant. But it's not. It's a regular dead ant with a parasitic fungus growing out of its head.

The fungus, in the genus Ophiocordyceps, didn't wait until the ant was dead to make a home inside its body. In fact, the fungus was the killer. When the ant was first infected with the fungus, it broke from its usual behaviors and climbed up to a high leaf. Then it clamped its jaws down, anchoring its body to the leaf, and died. Now in an advantageous spot for reproduction, the fungus sprouted a long, spore-bearing structure from the ant's head that will shower spores onto new ant prey below.

Parasitic fungi--even mind-controlling parasitic fungi--are nothing new to science. There are around 140 species in the Ophiocordyceps genus alone. What's new is that Penn State entomologist David Hughes and colleagues took a closer look at one species, Ophiocordyceps unilateralis, and discovered that it's actually, um, four species.

In the Brazilian rainforest, researchers collected infected carpenter ants (easily spotted by the filaments bursting out of their joints or stalks emerging from their heads). 
On close inspection, they found that O. unilateralis could be divided into four clear subtypes with different appearances. They gave each type a new species name, and intend to study the fungal DNA to confirm the differences they found.

Since the four species showed up in different species of carpenter ants, Hughes writes, "It is tantalizing to speculate that each species...may be attacked by a distinct species of Ophiocordyceps." More research will be needed to show whether that's really true. As for the mind-controlling fungi that attack wasps, flies, and other insects, are they equally specialized? How many insect species have a dedicated parasitic-fungus species? There may be a whole world of fungi out there that have evolved in parallel to the insect world: an entire tree of life dedicated to getting inside other life-forms' heads.

That should give you something to think about. Just don't get the idea to climb up to a high branch and bite down.


Images: David Hughes

Beating the Odds

Sometimes extinction can be a blessing. Aren't you glad this 500-million-year-old "walking cactus," for example, isn't alive today? It lived on the bottom of the ocean, to be fair. But just knowing it was there would have bothered me.

Conservationists have been speculating for years that we're in the midst of a mass extinction. In the planet's history, five of these events have occurred. To qualify, three-quarters of all species on Earth must be wiped out. The most recent mass extinction was the one that did in the dinosaurs. Prior to that, incidents such as global cooling or global warming served to wipe out huge numbers of species. And before any of those events, when the planet was occupied by simple single-celled creatures, the rise of the first photosynthesizers released oxygen into the atmosphere and destroyed most other forms of life.

So Earth is no stranger to slate-wiping events. But the great extinctions of the past occurred over hundreds of thousands, or millions, of years. Are humans, by spreading across every surface on Earth and pushing out the animals and plants that lie in our path, causing a new extinction event that's accelerated beyond anything the planet has seen before?

Anthony Barnosky, a paleobiologist at UC Berkeley, says yes. Barnosky and his colleagues compared the current rate of extinction among mammals to their historical extinction rate (since mammals are well catalogued today and well represented in the fossil record). They also examined the historical extinction rates of groups such as amphibians and birds that have been thoroughly assessed by the International Union for Conservation of Nature (IUCN), the group that labels species as endangered. Rates of extinction today, they found, are clearly higher than normal historic rates.

The researchers then compared all of these findings to the rates of species loss that drove the mass extinctions of the past. To project future extinctions, they looked at animals that are currently "threatened"--labeled by the IUCN as critically endangered, endangered, or vulnerable (more on that in a moment). If all threatened animals became extinct in the next hundred years, and we carried on at the same rate of species loss afterward, it would take between 240 and 540 years for 75% of species to be wiped out. That is, within just a few centuries, we could see a legitimate mass extinction.

The good news is that this outcome is far from certain. While a "critically endangered" species is defined as having only a 50% chance of surviving the next ten years--meaning its prospects for the coming century are pretty grim--a "vulnerable" species is considered to have only a 10% chance of extinction over the next hundred years. So for all currently threatened species to be gone within a hundred years would be, by the IUCN's definitions, very unlikely.

The point stands, though. Even if only the critically endangered animals disappear in the next hundred years, and if that rate continues, it will take some hundreds or thousands of years for us to reach the 75% mark--rather than the hundreds of thousands or millions of years seen in the five mass extinctions. This is species loss at a completely unnatural rate.

And it's our fault, in case you were unclear. The authors list changing atmospheric conditions, global warming, habitat loss, pollution, overhunting, overfishing, invasive species (carried by humans to places they don't belong) and "expanding human biomass" as reasons for the extinctions. The sheer weight of us on the world is, it seems, too much. But the future isn't certain. If we care enough, we might be able to beat the odds.

Image: Jianni Liu

Botswanavision

Do you ever find yourself squinting into the glare of your computer screen around 4 PM and thinking that your eyes aren't built for this? You're right, of course. The human eye evolved on the African savanna. This is what it's built to see:

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Scientists from the University of Pennsylvania and elsewhere took about 5,000 digital photos in a Botswana savanna. They captured natural scenes at various times of day, from sun-baked vistas to up-close tree bark to fresh elephant dung, and compiled the images into a publicly available database.

Clicking through the albums may make you feel overheated, but it also simulates a pleasant stroll through the savanna. (Spoiler alert: baby baboons!)

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The researchers used this database to investigate the evolution of the human eye. Specifically, they wanted to find the logic behind how our color-sensing machinery is set up.

Our eyes detect color using cone cells, which come in three types: one that detects light at short wavelengths (blue), one for medium wavelengths (green), and one for longer wavelengths (red). The three types of cones aren't distributed evenly across the retina, though. The blue-detecting cones are rare, and mostly exist around the outer edges of the retina. The red and green cones are much more common, but the ratio between them varies widely from person to person.

For each of the scenes in the Botswana photo database, scientists calculated how much light of different wavelengths would be reaching the viewer's eye. Based on those numbers, they mathematically determined the most efficient distribution of cone cells in the retina. They found that blue-detecting cones couldn't pick up as much information as the red or green cones (which explains why we don't make very many of these cells) but were most useful at the periphery of the eye. The red and green cone cells, though, would be about equally useful at picking up information from these scenes. That explains why humans can have widely varying ratios of red to green cone cells without an effect on their vision.

Though they may seem disorganized, our retinas have evolved to efficiently gather information from our environment--or our ancestral savanna, anyway. Future research might address how our eyes handle other environments. Additionally, the authors say that knowing how to build eyes efficiently might help us create better robots. Not having had the benefit of evolution, today's robots can't see nearly as well as we can.

Photos: University of Pennsylvania.