Researchers at the Great Lakes Environmental Research Laboratory borrowed some code from the designers who made this incredible wind map to create the world's first beautiful water current map. The image above is just a snapshot--check out the animated one here. Totally mesmerizing.

Today on Mars, Curiosity is cleaning itself out and preparing to study some sand. This image from Curiosity's Mast Camera shows the rover just after it discarded a soil sample as part of its first decontamination exercise. The rover's Collection and Handling for In-Situ Martian Rock Analysis (CHIMRA) tool on the end of its arm had just finished shaking some scooped-up Martian soil into the rover's science-sampling chambers. You can see some dirt left behind in the delivery tube, which is magnified at bottom right.

The sand is used to scrub the internal surfaces of the rover, serving as a quality-assurance protocol just in case anything from Earth was left over in there. Then the rover spits the sample back out.

When the decontamination process has been performed three times and actual sample distribution is ready, the rover will send sand to its Chemistry and Mineralogy (CheMin) and Sample Analysis at Mars (SAM) instruments.

This image was taken by Curiosity's right Mast Camera on October 10, the 64th sol since Curiosity landed in Gale Crater. Scientists white-balanced it to show the scene as it would appear under Earth-like lighting conditions--Mars is much less sunny, being a few hundred million miles further from our star.

Today in faulty causality: A study has found that a country's consumption of chocolate is directly correlated to the number of Nobel laureates it has produced. Leading the world in both chocoholism and Nobels: the Swiss, followed by the Swedes and the Danes. The U.S. would have to consume an additional 275 million pounds of chocolate per year to catch up (still no word on what benefits salt, a preponderance of processed foods, and trans-fats impart to a nation).

The correlation here is false, of course, and that's precisely why the study was published. New York physician Franz Messerli noticed the correlation and published the study to show how p-values--a statistical tool that nearly all medical studies employ to prove the veracity of the causal relationships they describe--can be seriously flawed.

P-values essentially measure the probability that a given result will be as "extreme" as the observation if indeed there is no real correlation. It's basically a test for randomness and a way for scientists to try to filter raw coincidence from their data. But in the case of the chocolate-to-Nobel correlation, Messerli calculated the p-value at 0.0001. That means the odds that this correlation is purely due to chance is just one in 10,000.

But Messerli himself calls the result "a complete nonsense correlation." While there could be some kind of indirect correlation--chocolate is a luxury good after all, so one could assume that countries rich in chocolate are also rich in other things, like health care, education, and other factors that might influence a person's chance of rising to Nobel status--there is no real established reason to believe that overall chocolate consumption (even dark chocolate, which has been shown in some studies to benefit the brain) generates Nobel laureates at an increased rate. Even the perceived link to wealth is incidental rather than causal. As a stand-alone finding, it is meaningless.

"Scientists look at hundreds and hundreds of different things, and every once in a while they will find two things that are surprisingly correlated with each other, and then they will say, 'Look at those very strong correlations and how important that is,'" American physicist and 2001 Nobel physics prize winner Eric Cornell told Reuters Health. "But what they don't do is tell you about all the different things that aren't correlated."

The lesson here: Brush up on your Nassim Nicholas Taleb and don't believe everything you read in the media. Some correlations are tempting and even statistically verifiable. But that doesn't necessarily make them, or the research they underpin, the undisputed truth.

[Reuters Health]

WHAT'S NEW

The big deal about this stove compared to other small camp stoves? Power. The BioLite has a USB port to charge your gadgets from excess heat generated from wood fires.

The CampStove's orange module houses a thermoelectric element, a battery, a fan, and a microprocessor. The microprocessor tweaks power distribution as needed to charge the battery or connected device. When you burn wood in the chamber, a copper probe transfers heat to one side of the element, while on the other side cool air provides a differential that enables ions to jump sides and generate electricity. The electricity powers a fan that pushes air through vents that stoke a vortex of wood blaze. It's so efficient you can use leftover electricity to charge devices while you cook a meal.

WHAT'S GOOD

As a stove: It's small and attractively designed, made of steel and orange plastic. Mine weighed in at two pounds two ounces, nice and light, and I like the way it stands up--three aluminum legs fold out on hinges like something designed for Curiosity.

Typical wood fires are not the most pleasant to cook around, due to smoke (ow, my eyes!). The BioLite produces smoke when the fire is first lit, but once the fan starts to direct the air flow, there's almost no smoke and zero embers fly out.

The BioLite is perfect to boil water in a pot. I prefer my camping meals light and simple to prepare, so this stove is great for heating up water to rehydrate freeze-dried meals. The fire mellowed when we pressed the power button to set the fan mode from high to low and we even fried eggs in a pan. For tea, I boiled a cup of water in roughly two minutes, which would have easily taken three times longer with my alcohol stove. (Some more data: bringing two cups of 53-degree water to a vigorous boil took three minutes.)

The stove's also smart--sometimes even smarter than you. When a user tries to turn off the fan before the chamber is cool enough, the fan turns back on - a sure sign you should avoid touching the chamber. The power module can be touched throughout use and only reached about 125 degrees - just warm to the touch. Once the chamber cools, just dump the small bit of ash leftover. The chamber itself is steel, so you can throw it in the dishwasher back in civilization.

As a charger: Let the fire burn for a few seconds, then hit the single button on the power module, and it all starts happening. A few minutes later, a light around the USB port turns green, and your USB-based gadget starts to charge. Sweet! Charge times depend on the device--mostly, the capacity of the battery and the speed of the USB connection. It's not going to bring your phone to 100 percent in the time it takes to boil water, but our testing showed that charging during a regular cook--around 20-25 minutes--increases the battery on a smartphone (we tested with an LG Optimus V) between 6 and 12 percent, giving you about an hour of talk time. Not bad, considering at its hottest the BioLite delivers only four watts.

Compared to an alcohol stove, we like the size much better--it's wider, so it's easier to balance pots, pans, and kettles, though the overall size is also bigger. Not really having to worry about fuel is nice, too, since it's wood-fired, and though it does get a little sooty, it beats an alcohol stove to boil water in most conditions. It also turned out to be a really cool little wood stove for a New York City roof. Using wood pellets (I found mine at Trader Joe's), the stove was perfect to grill a steak or a burger.

BioLite CampStove Demo & Story from BioLite on Vimeo.

WHAT'S BAD

I took the CampStove out on multi-day canoe camping trips. One trip was a constant deluge of rain and all my tinder and kindling were soaked. The fan helped produce enough heat to boil a couple liters of water but took nearly 30 minutes. To be fair, I likely would have never gotten a boil with a wood fire without the CampStove. (Fun note: I've learned since then that chunks of wood from inside fallen logs stay pretty dry even in the rain.)

The first time, I neglected to charge the power module (as recommended) before leaving civilization, so that may have made matters worse. The battery needs to be conditioned with a charge from a USB port from a computer or most adaptors the first time it's used. You only need to condition the battery for the first use or after a long time on the shelf, so that's just once at the beginning of a season.

Also, if the fire starts to falter before you're done cooking, you have to lift the pot or pan to sneak some more tinder into the chamber. That's a minor annoyance, but one that can be avoided if the first fill of kindling is fairly dense and you're just cooking for one or two people. And though it's an efficient stove, the CampStove fire is only four inches in diameter. You won't grill a porterhouse on it or vegetable kebabs - though BioLite plans to release a grill add-on for spring 2013.

THE PRICE

$129 on BioLite's site. That's more than a little alcohol stove, which usually cost around 40 bucks or even less. The CampStove's price puts it at the same price point as some really nice compressed-fuel stoves. But you're getting a lot more for your money--and a compressed-fuel stove won't charge your iPhone.

THE VERDICT

When I first saw the CampStove on Kickstarter, I smirked and tossed the idea in the "gimmicks for iPhone" category. But then I learned about the science that powers the little machine, and was intrigued enough to burn some wood in it. I'm glad I did. I think campers and especially backpackers will find this stove a reliable tool for the trail. If that weren't enough, at home, the CampStove perched on a shelf doubles almost as a functional piece of modern art that, at the very least, encourages you to get outside into nature.

Hundreds of pages of fairly damning evidence came out against Lance Armstrong this week, accusing him of not only using performance enhancements but also of being "a bully" and developing "a culture of doping." It all leads to an obvious question: What about me? If I got up from my desk and injected some high-octane Armstrong juice, could I, too, win the Tour de France?

No. But if I replicated his (alleged) process, I might be able to get up a mountain I couldn't get up before.

Here's a list of some stuff Armstrong is accused of doing--call it the Armstrong Cocktail. Let's go down the list.

BLOOD DOPING

This is something of a catch-all term, says Don Catlin, a pharmacologist at the University of California, Los Angeles. Most of the time, people use it to describe a blood transfusion process that can improve athletic performance. The general idea is to take blood--either from yourself (an autologous transfusion) or--if you're in mid-Tour, say--from another, compatible donor (a homologous transfusion). You then concentrate it to separate the red blood cells, and inject it before a race. (Armstrong is accused of using the autologous method.) Either way, the extra red blood cells can increase endurance quite a bit--according to one study, improving stamina up to 34 percent. Erythropoietin (EPO), which was also mentioned in the allegations, is another way of increasing the concentration of red blood cells in your blood. It's a naturally occurring hormone, usually given to anemic patients, that can stimulate the body to create more red blood cells.

For men, standard hematocrit (the proportion of red cells to other stuff) is about 44 to 45 percent. Most testing regulations, Catlin says, dictate that competitors will be flagged if hematocrit is above 50 percent. So: "They aim for 49 and a half percent."

How much would I improve?

Potentially, my stamina could increase 34 percent. That could make the climb up a hill a lot easier.

TESTOSTERONE

This is complicated. Conventional wisdom dictates that you won't get anywhere taking testosterone or other steroids if you aren't already training, but a few studies have come out contradicting that assessment, says Charles Yesalis, an emeritus professor of sports science at Pennsylvania State University. But either way, it's going to be a much bigger increase for people who train regularly, or even semi-regularly, than for people who don't. Similarly, women, who produce between one-tenth and one-fifteenth the testosterone of men, will see a much bigger increase in performance, Yesalis says.

Even for the regular person, there's some variability in how you'll react to steroids--it might be a huge increase for someone, and next to nothing for someone else. But even the low end could have "a profound effect," Yesalis says. Catlin estimates that between a 5 and 15 percent improvement in cycling speed would be "expected," although, again, that could go up or down depending on how the person reacts to the dope. (We don't know exactly why, physiologically, people vary in their reactions, but Yesalis says there's going to be some increase for anyone.)

How much would I improve?

Let's take the low end: 5 percent. I'm just an average cyclist, after all. Still, that shaves quite a few hours off my completion of the 21-day Tour.

HUMAN GROWTH HORMONE (HGH)

This one's a no-go in some ways: Athletes use it, but this hormone, which makes it easier for competitors to increase muscle mass over the long term, hasn't been definitively proven to increase strength or endurance. Although one study did find a four percent increase in sprinters' performance, what's more commonly reported that is that it decreases the recuperative time between training; that's widely, if anecdotally, reported, Yesalis says. It's tough to say how much that adds up to mathematically, but being able to train more could increase my performance, if I felt like training.

How much would I improve?

Hard to say.

CORTICOSTEROIDS (CORTISONE)

This is used as a way to mask pain caused by workouts, thereby letting a cyclist (or whoever) compete more efficiently. Generally, they're a way to reduce inflammation in people experiencing pain, but they can give athletes a boost in the same way by letting them keep going--no pain, lots of gain. Hard to quantify, but I definitely plan on using plenty.

How much would I improve?

Same as above. Inconclusive.

SALINE AND PLASMA INFUSIONS

This doesn't directly give athletes any increase in performance; it's more of a way to foil drug tests. When competitors are blood doping, sometimes they "overshoot," Catlin says: The amount of red blood cells goes over that 50 percent mark (or whatever the mark is) and they'll be sit out of competition. So, to balance out the equation, dopers will add saline or plasma to their system, bringing the proportion back down to acceptable (but still performance-enhancing) levels.

How much would I improve?

None.

SO CAN I BIKE UP A MOUNTAIN YET?

Sure! Especially if I aim for a mountain that I can bike up already.

It's hard to say exactly how these boosts "stack," Yesalis says--that is, whether two percentage increases can be combined neatly or whether you have to factor them into a complicated curve. For the most part, these are small increases, which can make a lot of difference in a top-tier race that comes down to a second or, in longer races, the minute.

To get up that mountain, I'd need to be able to climb most of the mountain (80 or 90 percent maybe) without help. If there's a mountain that's your own personal white whale, that you're within a few more pushes toward slaying, the Armstrong Cocktail could do it.

Remember, though, that it also depends on the person. A woman would get more out of the testosterone increases than a man; some people will see more improvement from steroid use in general; a regular cyclist who continues training while doping will see more of an improvement. Will I see a boost from this? Yes, probably. How much will it be? Not as much as Lance (allegedly) saw.

Conclusion? Probably not worth it. I am not going to transfuse my blood just yet.

[data sources: Nature, Time, HowStuffWorks]

DARPA, the military's crazyscience wing, is known for many things--but one of our favorites is the Grand Challenge, which demonstrate the power of crowdsourcing and competitiveness to push technology forward. Now DARPA needs our help. What should the next Grand Challenge be about?

Click to launch the photo gallery

Grand Challenges are ambitious but achievable, imagination-inspiring but believable, and they have to have results that are measurable--like sequencing the human genome, or landing a couple of people on the moon and returning them safely home. Past DARPA Grand Challenges have led to self-driving cars, translating messages on shredded paper, and more--soon, even humanoid robots that can work alongside human warfighters.

DARPA wants some help picking a new one, and there's a formal request for proposals. So we went ahead and made some of our own. Visit the gallery to see them and add yours in the comments.

Sometimes, when your cat comes back from...wherever cats go, you don't have to guess what it's been up to: the headless mouse on your doorstep (or your living room floor, or your bed) is a dead giveaway. But what about all those other times, when the cat returns sans spoils? Has it been killing stuff then, too?

Matthew Inman presents some new findings on the American house cat's killing habits in this infocomic at TheOatmeal.com.

We invented the Internet here in the U.S., but other countries have long since improved on our work. We're 13th worldwide in average connection speed, and we usually pay more to access those slower connections. In some parts of the country, a world-class connection is unavailable at any price.

Our system lags in part because it's physically bound to its own long history. A century ago, for instance, it made sense to route telegraph and phone lines alongside train tracks, where someone had already negotiated right-of-way, but that means 21st-century data packets now run through networks optimized for 19th-century railroads. No wonder Latvia, South Korea, and others are pulling ahead: They're building from scratch.

Several recent experiments are showing how we could start over with a new system ourselves-one that's not just faster, cheaper, and more accessible, but also far less likely to become outmoded.

The key is wireless mesh networks. Engineers from Afghanistan to Brooklyn are studying how to use these networks-made up of hundreds of Wi-Fi routers linked by custom software-to achieve a variety of ends: connecting impoverished communities, creating off-the-grid phone service, linking activists in countries where the Internet is censored. Routers are cheap and constantly improving, so the networks are easy to upgrade. And because they connect to one another independently of the phone or cable company, access doesn't have to cost anything. The problem, for now, is that people can't reach anyone outside the network. If they want to send an e-mail to their grandmothers, they still have to send a check to the phone company first.

Make the network big enough, though, and it could in theory replace the commercial Internet. We'd just have to blanket the country with millions of little routers. How could we achieve such a feat? We already have. Phones, laptops, cameras, coffeemakers, game consoles, and millions of other gadgets all come with Wi-Fi right now and are capable of relaying data from one to the next. All that's missing is a common protocol.

So what if-and granted, this is a big if-manufacturers agreed on that protocol? What if they began building common mesh-network drivers into every Wi-Fi device? Like the World Wide Web, the resulting network would at first be a mere novelty. But as users began to trust the system, they would find more reasons to connect-it would be free, after all-and eventually it might reach the same critical mass the Web did a decade ago. Best of all, since the "infrastructure" would consist only of consumer devices, it could improve as quickly as they do.

A worldwide communications system made entirely of gadgets sounds improbable, but the idea that our whole economy would migrate to the Web once seemed unlikely, too. When you open closed systems, things happen fast.

Luke Mitchell (luke.mitchell@popsci.com) is the magazine's Ideas Editor

It's a shame that you can't actually fight fire with fire. That would be cool. And dangerous. Fire's great when you're studying the behavior of a flame on the International Space Station or making your animatronic dragon more realistic, but it's even more great when you're not being burned alive, so be cool about fire safety.

For National Fire Prevention Week, we bring you fire safety tips and technology courtesy of PopSci writers and fire enthusiasts past. Be careful about that watch you're wearing--it could erupt into flames!

See the gallery.

A "mild" is a type of ale first produced in the 1700s in England. The term "mild" originated to mean a young beer (meant to be drunk fresh), as opposed to a beer that you could age for a while in the barrel. A modern mild has a strong malt character, is dark(er) in color and generally clocks in under 4% alcohol by volume (ABV), which means it's a session beer, something you can drink a few of in a sitting without getting completely hammered. 

My spouse Doug and I brewed the Marathon Mild just before Doug ran his debut marathon last November. Coincidentally, it was our 26th batch of beer (a marathon is 26.2 miles), and as Doug slogged through the streets of New York City, it sat in our bedroom closet, happily fermenting away. It was something of a pity that the Marathon Mild wasn't ready to drink right after the marathon, but Doug made do drinking beers from earlier batches (if I recall correctly, a juniper pale ale, a black saison and a dry-hopped regular saison) while he iced his knees. We drank the 5-gallon batch of Marathon Mild over Thanksgiving with family. 

So why am I sharing Marathon Mild with you today? Because Doug just completed his second marathon (Chicago), Thanksgiving is around the bend, and if you're not interested in the former, at least the latter will make you want to drink.

There is one more reason: Right now is hop-harvest season and the Centennial hop, a core ingredient in Marathon Mild, is big this year. In Washington, production of Centennial hops is expected to double (641 acres to 1,365), according to the USDA. (The official harvest numbers of all of your favorite hop varietals won't be published until December, but you can get the data on acres planted from the USDA fact sheet.) Centennial is such a great all-around hop, and I'm happy to see increased production because it means that 1.) we're likely to be able to get it regularly, unlike perennially sold-out Simcoe and 2.) it means that more professional brewers are using it. I've found that my enjoyment of certain beers is directly related to the hop variety used. There are some hop varietals, such as Cluster, whose organoleptic properties I just cannot abide.

Depending on a variety of factors, Doug and I mix up our brewing between all-grain and partial-mash. "All-grain" means exactly that: all of the sugar comes from kernels of barley that we have to process ourselves. "Partial-mash" means that some of our sugar comes from kernels of barley, and some of it comes as malt extract (that means that someone else has processed the kernels for us and concentrated all of the malt sugars into a syrup). It's possible to brew with just extract, and novice homebrewers should start with that--mashing is a finicky process best helped along by drinking a bottle of already-made homebrew. More-experienced homebrewers like the versatility of choosing exactly which grains go in their beer. That said, there are plenty of experienced homebrewers who stick with extract brewing because it's easy to brew consistently good beers with it.  

This mild recipe is all grain and is based on a recipe for a JW Lees Best Mild from 1952. Doug and I brewed the 1952 recipe a year earlier, and wanted to play with the proportions a bit. I left out the invert sugar and the black malt thinking that I might get more malt character and a little less roast character--I wasn't looking for a dark, coffee-like flavor in the palate. I used Centennial hops because that is what we had on hand, though any relatively clean bittering hop will do. Aim for 14 IBU.

Marathon Mild (5-gallon all-grain batch):
6 lbs Maris Otter malt
1 lb Crystal 120
8 oz brown malt
2 oz chocolate malt
0.4 oz Centennial Hops (whole hops - 10.5% alpha acids)

1. Mashed the grains in 9.75 quarts of water at 150F for an hour. Efficiency was around 65%.

2. Sparged with 168F water in two steps: 1.88 gal and 3.39 gal. 

3. Boiled with Centennial hops for 60 minutes. No aroma hops. Pretty sure we used Whirlfloc.

OG: 1.039 FG: 1.010 ABV: 3.8%.

As an aside, Doug and I typically use BeerSmith when creating recipes.

To the neophyte homebrewers, I am sure that some of the stuff I just posted is obscure gobbledygook. For those who are just starting or who want to keep up on the homebrewing side, I recommend two books. The first is the classic Joy of Homebrewing by Charlie Papazian. The second is How to Brew by John Palmer. I especially recommend this second one for those who are science-minded. I appreciate Papazian because he takes a lighthearted approach to the hobby and, let's face it, we all need some levity in our lives. But Palmer's book is all about grokking brewing on a more mechanistic level, which is what this column is going to be all about. The entire book is available as hyperlinked chapters online, but I found it most useful as a physical object to read in my spare time.  

Next week on BeerSci: I fall down the rabbit hole researching the S. cerevisiae genome.

P.S. Follow me on Twitter! @BeerSci will feature beer-related mutterings, brew reviews and embarrassing photos, all in 140 characters or less.

Want to win this conspiring Baarbarian illustration on a T-shirt? It's easy! The rules: Follow us on Twitter (we're @PopSci) and retweet our This Week in the Future tweet. One of those lucky retweeters will be chosen to receive a custom T-shirt with this week's Baarbarian illustration on it, thus making the winner the envy of friends, coworkers and everyone else with eyes. (Those who would rather not leave things to chance and just pony up some cash for the T-shirt can do that here.) The stories pictured herein:

• The More Chocolate A Nation Eats, The More Nobel Prizes It Gets
• Daily Infographic: What Is The Real Status Of The Polar Bears?
• Meet Polaris, The First Ice-Drilling Lunar Prospector-Bot
• With Basic Physics, You Can Beat the House At Roulette

And don't forget to check out our other favorite stories of the week:

• Should Satellite Map Data Be Uncensored For All To Enjoy?
• 5 Secrets Of A Successful Space Dive
• Remember When The Nobels Used To Be Inspiring?
• GameSci: Where's Our Virtual Reality?
• 1 In 10 People Believes The World Will End In 2012 [Infographic]
• The Alien Origins Of Felix Baumgartner's Attempt To Skydive From 23 Miles Up
• Out Today: 'Modernist Cuisine At Home,' Now Smaller And Cheaper
• Chanting "Party Hard!" While A Man Gets Zapped With A Million Volts
• You Built What?!: A Tesla Coil Gun That Produces Foot-Long Sparks
• FYI: If I Did A Bag Of Lance Armstrong's Blood, Could I Bike Up A Mountain?
• BioLite CampStove Review: Cook Your Food And Charge Your Gadgets In the Wilderness
• How Do We Know We're Not Living Inside A Massive Computer Simulation?
• The 'Impossible' Instant Camera: PopSci Breaks Open The Polaroid SX-70
• Everything You Need To Know About The Deadly Meningitis Outbreak
• Inside The Swarming Quadrotor Lab Of KMel Robotics
• Dear Mystery Algorithm That Hogged Global Financial Trading Last Week: What Do You Want?

Click here to see the gallery.

It's largely about how it feels in the mouth. Once a piece of cheddar has been heated to around 150°F, the matrix of milk proteins that provide its structure begins to break down, and the cheese takes on a creamy texture that many people find appealing.

What defines creaminess, and why do people find it so appetizing? That's a mystery. But a group of scientists based in the Netherlands, using experimental vanilla custard, found that the dessert's creaminess depends on factors including its viscosity, homogeneity, and texture and surface appearance. One of the scientists, René de Wijk of Wageningen UR's Food & Biobased Research division, says test subjects were especially inclined toward custards that produce lower friction in the mouth. The same factors may apply to cheese, de Wijk says. Harold McGee, author of On Food and Cooking: The Science and Lore of the Kitchen, adds that the warmth of melted cheese provides its own source of pleasure.

Taken together, all the sensations associated with melted cheese-smoothness, gooeyness, and warmth-connote a fatty treat. And humans love fat. Ivan de Araújo, a researcher at Yale, has studied how the nervous system responds to fatty foods. Possibly as a result of evolution or individual learning, he says, receptors in our mouths are keyed in to the texture of oily, calorie-dense foods. "And that perception may be an indicator, either innate or not," he says, "of the presence of fat."

tl;dr: Our nervous system is stimulated by creamy textures.

Have a burning science question you'd like to see answered in our FYI section? Email it to fyi@popsci.com.

In June 2008, a Dutch woman named Astrid Joosten left the Netherlands with her husband for an adventure vacation in Uganda. It wasn't their first trip to Africa, but it would be more consequential than the others.

At home in Noord-Brabant, Joosten, 41, worked as a business analyst for an electrical company. Both she and her spouse, a financial manager, enjoyed escaping Europe on annual getaways. In 2002, they had flown to Johannesburg and, stepping off the airplane, felt love for Africa at first sight. On later trips they visited Mozambique, Zambia, and Mali. The journey to Uganda in 2008, booked through an adventure-travel outfitter, would allow them to see mountain gorillas in the southwestern highlands of the country as well as some other wildlife and cultures. They worked their way south toward Bwindi Impenetrable Forest, where the gorillas reside. On one day, the operators offered a side trip, an option, to a place called the Maramagambo Forest, where the chief attraction was a site known as Python Cave. African rock pythons lived there, languid and content, grown large on a diet of bats.

Joosten's husband, later her widower, is a fair-skinned man named Jaap Taal, a calm fellow with a shaved head and dark, roundish glasses. Most of the other travelers didn't fancy this Python Cave offering, he told me later. "But Astrid and I always said, ‘Maybe you come here only once in your life, and you have to do everything you can.' " They rode to Maramagambo Forest and then walked a mile or so, gradually ascending, to a small pond. Nearby, half-concealed by moss and other greenery, like a crocodile's eye barely surfaced, was a low, dark opening. Joosten and Taal, with their guide and one other client, climbed down into the cave.

The footing was bad: rocky, uneven, and slick. The smell was bad too: fruity and sour. Think of a dreary barroom, closed and empty, with beer on the floor at three a.m. The cave seemed to have been carved by a creek, or at least to have channeled its waters, and part of the overhead rock had collapsed, leaving a floor of boulders and coarse rubble, a moonscape, coated with guano like a heavy layer of vanilla icing. It served as a major roosting site for the Egyptian fruit bat (Rousettus aegyptiacus), a crow-size chiropteran that's widespread and relatively abundant in Africa and the Middle East. The cave's ceiling was thick with them-many thousands, agitated and chittering at the presence of human intruders, shifting position, some dropping free to fly and then settling again. Joosten and Taal kept their heads low and watched their step, trying not to slip, ready to put a hand down if needed. "I think that's how Astrid got infected," Taal told me. "I think she put her hand on a piece of rock, which contained droppings of a bat, which are infected. And so she had it on her hand." Maybe she touched her face an hour later, or put a piece of candy in her mouth, "and that's how I think the infection got in her."

No one had warned Joosten and Taal about the potential hazards of an African bat cave. They knew nothing of a virus called Marburg (though they had heard of Ebola). They only stayed in the cave about 10 minutes. They saw a python, large and torpid. Then they left, continued their Uganda vacation, visited the mountain gorillas, took a boat trip, and flew back to Amsterdam. Thirteen days after the cave visit, home in Noord-Brabant, Joosten fell sick.

No one had warned Joosten and Taal about the potential hazards of an African bat cave.At first it seemed no worse than the flu. Then her temperature climbed higher and higher. After a few days, she began suffering organ failure. Her doctors, knowing of her recent time in Africa, suspected Lassa virus or maybe Marburg. "Marburg," said Taal, "what's that?" Joosten's brother looked it up on Wikipedia and told him: "Marburg virus: It kills, could be big trouble." In fact, it's a filovirus, the closest relative to the ebolaviruses (of which there are five species, including the most infamous, Ebola). Marburg was first discovered in 1967, when a group of African monkeys, imported to Marburg an der Lahn, in western Germany, for medical research uses, passed a nasty new virus to laboratory workers. Five people died. In the decades since, it has also struck hundreds of Africans, with a case fatality rate of up to 90 percent.

The doctors moved Joosten to a hospital in Leiden, where she could get better care and be isolated from other patients. There, she developed a rash and conjunctivitis; she hemorrhaged. She was put into an induced coma, a move dictated by the need to dose her more aggressively with antiviral medicine. Before she lost consciousness, though not long before, Taal went back into the isolation room, kissed his wife, and said to her, "Well, we'll see you in a few days." Blood samples, sent to a lab in Hamburg, confirmed the diagnosis: Marburg. She worsened. As her organs shut down, she lacked for oxygen to the brain, she suffered cerebral edema, and before long Joosten was declared brain-dead. "They kept her alive for a few more hours, until the family arrived," Taal told me. "Then they pulled the plug out, and she died within a few minutes."

A horse dies mysteriously in Australia, and people around it fall sick. A chimpanzee carcass in Central Africa passes Ebola to the villagers who scavenge and eat it. A palm civet, served at a Wild Flavors restaurant in southern China, infects one diner with a new ailment, which spreads to Hong Kong, Toronto, Hanoi, and Singapore, eventually to be known as SARS. These cases and others, equally spooky, represent not isolated events but a pattern, a trend: the emergence of new human diseases from wildlife.

The experts call such diseases zoonoses, meaning animal infections that spill into people. About 60 percent of human infectious diseases are zoonoses. For the most part, they result from infection by one of six types of pathogen: viruses, bacteria, fungi, protists, prions, and worms. The most troublesome are viruses. They are abundant, adaptable, not subject to antibiotics, and only sometimes deterred by antiviral drugs. Within the viral category is one particularly worrisome subgroup, RNA viruses. AIDS is caused by a zoonotic RNA virus.
So was the 1918 influenza, which killed 50 million people. Ebola is an RNA virus, which emerged in Uganda this summer after four years of relative quiescence. Marburg, Lassa, West Nile, Nipah, dengue, rabies, yellow fever virus, and the SARS bug are too.

Over the last half dozen years, I have asked eminent disease scientists and public-health officials, including some of the world's experts on Ebola, on SARS, on bat-borne viruses, on HIV-1 and HIV-2, and on viral evolution, the same two-part question: 1) Will a new disease emerge, in the near future, sufficiently virulent and transmissible to cause a pandemic capable of killing tens of millions of people? and 2) If so, what does it look like and from where does it come? Their answers to the first part have ranged from maybe to probably. Their answers to the second have focused on zoonoses, particularly RNA viruses. The prospect of a new viral pandemic, for these sober professionals, looms large. They talk about it; they think about it; they make contingency plans against it: the Next Big One. They say it might happen anytime.

To understand what killed Astrid Joosten, and to see her case within the context of the Next Big One, you need to understand how viruses evolve. Edward C. Holmes is one of the world's leading experts in viral evolution. He sits in a bare office at the Center for Infectious Disease Dynamics, which is part of Pennsylvania State University, and discerns patterns of viral change by scrutinizing sequences of genetic code. That is, he looks at long runs of the five letters (A, C, T, G, and U) that represent nucleotide bases in a DNA or RNA molecule, strung out in unpronounceable streaks as though typed by a manic chimpanzee. Holmes's office is tidy and comfortable, furnished with a desk, a table, and several chairs. There are few bookshelves, few books, few files or papers. A thinker's room. On the desk is a computer with a large monitor. That's how it all looked when I visited, anyway.

Above the computer was a poster celebrating "the Virosphere," meaning the totality of viral diversity on Earth. Beside that was another poster, showing Homer Simpson as a character in Edward Hopper's famous painting Nighthawks. Homer is seated at the diner counter with a plate of doughnuts before him.

Holmes is an Englishman, transplanted to central Pennsylvania from London and Cambridge. His eyes bug out slightly when he discusses a crucial fact or an edgy idea, because good facts and ideas impassion him. His head is round and, where not already bald, shaved austerely. He wears wiry glasses with a thick metal brow, and while he looks a bit severe, Holmes is anything but. He's lively and humorous, a generous soul who loves conversation about what matters: viruses. Everyone calls him Eddie.

"Most emerging pathogens are RNA viruses," he told me, as we sat beneath the two posters. RNA as opposed to DNA viruses, he meant, or to bacteria or to any other type of pathogen. To say that Eddie Holmes wrote the book on this subject wouldn't be metaphorical. It's titled The Evolution and Emergence of RNA Viruses, published by Oxford in 2009, and that's what had brought me to his door. Now he was summarizing some of the highlights.

There are an awful lot of RNA viruses, he said, which might seem to raise the odds that many would come after humans. RNA viruses in the oceans, in the soil, in the forests, and in the cities; RNA viruses infecting bacteria, fungi, plants, and animals. It's possible that every cellular species of life on the planet supports at least one RNA virus, though we don't know for sure because we've just begun looking. A glance at his virosphere poster, which portrayed the universe of known viruses as a brightly colored pizza, was enough to support that point. It showed RNA viruses accounting for at least half the slices. But they're not merely common, Eddie said. They're also highly evolvable. They're protean. They adapt quickly./>

Two reasons for that, he explained. It's not just the high mutation rates but also the fact that their population sizes are huge. "Those two things put together mean you'll produce more adaptive change," he said.

RNA viruses replicate quickly, generating big populations of viral particles within each host. Stated another way, they tend to produce acute infections, severe for a short time and then gone. Either they soon disappear or they kill you. Eddie called it "this kind of boom-bust thing." Acute infection also means lots of viral shedding-by way of sneezing or coughing or vomiting or bleeding or diarrhea-which facilitates transmission to other victims. Such viruses try to outrace the immune system of each host, taking what they need and moving onward quickly, before a body's defenses can defeat them. (The HIVs are an exception, using a slower strategy.) Their fast replication and high rates of mutation supply them with lots of genetic variation. Once an RNA virus has landed in another host-sometimes even another species of host-that abundant variation serves it well, giving it many chances to adapt to the new circumstances, whatever those circumstances might be.

Most DNA viruses embody the opposite extremes. Their mutation rates are low and their population sizes can be small. Their strategies of self-perpetuation "tend to go for this persistence route," Eddie said. Persistence and stealth. They lurk; they wait. They hide from the immune system rather than try to outrun it. They go dormant and linger within certain cells, replicating little or not at all, sometimes for many years. I knew he was talking about things like varicella zoster, a classic DNA virus that begins its infection of humans as chickenpox and can recrudesce, decades later, as shingles. The downside for DNA viruses, he said, is that they can't adapt so readily to a new species of host. They're just too stable. Hidebound. Faithful to what has worked in the past.

The stability of DNA viruses derives from the structure of the genetic molecule and how it replicates: It uses the enzyme DNA polymerase to assemble and proofread each new strand. The enzyme employed by RNA viruses, on the other hand, is "error-prone," according to Eddie. "It's just a really crappy polymerase," which doesn't proofread, backtrack, or correct erroneous placement of those RNA nucleotide bases, A, C, G, and U. Why not? Because the genomes of RNA viruses are tiny, ranging from about 3,000 nucleotides to about 30,000, which is much less than what most DNA viruses carry. "It takes more nucleotides," Eddie said-a larger genome, more information-"to make a new enzyme that works." One that works as neatly as DNA polymerase does, he meant.

These cases represent a pattern: the emergence of new human diseases from wildlife.And why are RNA genomes so small? Because their self-replication is so fraught with inaccuracies that, given more information to replicate, they would accumulate more errors and cease to function at all. It's sort of a chicken-and-egg problem. RNA viruses are limited to small genomes because their mutation rates are so high, and their mutation rates are so high because they're limited to small genomes. In fact, there's a fancy name for that bind: Eigen's paradox. Manfred Eigen is a German chemist, a Nobel laureate, who has studied the evolution of large, self-replicating molecules. His paradox describes a size limit for such molecules, beyond which their mutation rate gives them too many errors and they cease to replicate. They die out. RNA viruses, thus constrained, compensate for their error-prone replication by producing huge populations and achieving transmission early and often. They can't break through Eigen's paradox, it seems, but they can scoot around it, making a virtue of their instability. Their copying errors deliver lots of variation, and variation allows them to evolve fast.

"DNA viruses can make much bigger genomes," Eddie said. Unlike the RNAs, they're not limited by Eigen's paradox. They can even capture and incorporate genes from the host, which helps them to confuse a host's immune response. They can reside in a body for longer stretches of time, content to get themselves passed along by slower modes of transmission, such as sexual and mother-to-child. "RNA viruses can't do that." They face a different set of limits and options. Their mutation rates can't be lowered. Their genomes can't be enlarged. "They're kind of stuck."

What do you do if you're a virus that's stuck, with no long-term security, no time to waste, nothing to lose, and a high capacity for adapting to new circumstances? By now we had worked our way around to the point that interested me most. "They jump species a lot," Eddie said.

Whence do they jump? From one species of primate to another, from one rodent to another, from a prey animal into a predator, and so on. Such leaps probably occur often in the quiet isolation of forests and other wild habitats, and usually they go undetected by science. But sometimes the leap is from a nonhuman critter into a human. Then we notice.

The kind of animal that harbors a given virus is known as its reservoir host. Could be a monkey, a bat, maybe a rat. Within its reservoir host the virus lives quietly, in a sort of long-term truce, causing no obvious symptoms. Passage from one kind of host to another is called spillover. In the new host, the old truce doesn't apply. The virus may turn aggressive and virulent. If the new host is human, you've got a newly emerged zoonotic disease.

Spillover to humans, as Eddie Holmes noted, occurs more often among RNA viruses than other bugs. It brings creatures such as Lassa (first recorded in 1969), Ebola (1976), HIV-1 (inferred in 1981, isolated in 1983), HIV-2 (1986), Sin Nombre (the infamous American hantavirus, 1993), Hendra (1994), avian flu (1997), Nipah (1998), West Nile (1999), SARS (2003), and swine flu (2009) into people's lives. Marburg is just another of the leaping threats, rare but dramatic in its impact on humans. Why are these spillovers happening, ever more frequently, in what seems a drumbeat of bad news?

To put the matter in its starkest form: Human-caused ecological pressures and disruptions are bringing animal pathogens ever more into contact with human populations, while human technology and behavior are spreading those pathogens ever more widely and quickly. In other words, outbreaks of new zoonotic diseases, as well as the recurrence and spread of old ones, reflect things that we're doing, rather than just being things that are happening to us.

We have increased our human population to the level of seven billion and beyond. We are well on our way toward nine billion before our growth trend is likely to flatten. We live at high densities in many cities. We have penetrated, and we continue to penetrate, the last great forests and other wild ecosystems of the planet, disrupting the physical structures and the ecological communities of such places. We cut our way through the Congo. We cut our way through the Amazon. We cut our way through Borneo. We cut our way through Madagascar. We cut our way through New Guinea and northeastern Australia. We shake the trees, figuratively and literally, and things fall out. We kill and butcher and eat many of the wild animals found there. We settle in those places, creating villages, work camps, towns, extractive industries, new cities. We bring in our domesticated animals, replacing the wild herbivores with livestock. We multiply our livestock as we've multiplied ourselves, establishing huge factory-scale operations that contain thousands of cattle, pigs, chickens, ducks, sheep, and goats. We export and import livestock, fed and fattened with prophylactic doses of antibiotics and other drugs, across great distances and at high speeds. We export and import wild animals as exotic pets. We export and import animal skins, contraband bushmeat, and plants, some of which carry hidden microbial passengers. We travel, moving between cities and continents even more quickly than our transported livestock. We visit monkey temples in Asia, live markets in India, picturesque villages in South America, dusty archaeological sites in New Mexico, dairy towns in the Netherlands, bat caves in East Africa, racetracks in Australia-breathing the air, feeding the animals, touching things, shaking hands with the locals-and then we jump on our planes and fly home. We provide an irresistible opportunity for enterprising microbes by the ubiquity and sheer volume and mass of our human bodies.

Everything just mentioned falls under this rubric: the ecology and evolutionary biology of zoonotic diseases. Ecological circumstance provides opportunity for spillover. Evolution seizes opportunity, explores possibilities, and helps convert spillovers to pandemics. But "ecology" and "evolutionary biology" sound like science, not medicine or public health. If zoonoses from wildlife represent such a significant threat to global security, then what's to be done? Learn more. RNA viruses are everywhere, as Eddie Holmes has warned, and science has identified only a fraction of them. Fewer still have been traced to their reservoir hosts, isolated from the wild, grown in the lab, and systematically studied. Until those steps have been achieved, the viruses in question can't be battled with vaccines and treatments. This is where the field and laboratory scientists-veterinary ecologists, epidemiologists, molecular phylogeneticists, lab virologists-come in. If we're going to understand how zoonoses operate, we need to find these bugs in the world, grow them in cell cultures the old-fashioned way, look at them in the flesh, sequence their genomes, and place them within their family trees. It's happening, in laboratories and at field sites all over the world; but it's no simple task.

Astrid Joosten wasn't the only person in recent years to die of Marburg. In 2007, a year before her visit to Uganda, a small outbreak occurred among miners in roughly the same area. Just four men were affected, of whom one died. All of them worked at a site called Kitaka Cave, in the southwestern corner of Uganda.

Why are these spillovers happening, ever more frequently, in what seems a drumbeat of bad news?Soon after the news of the affliction got out, in August 2007, an international response team converged on Uganda to assist and collaborate with the Ugandan Ministry of Health. The group included scientists from the Centers for Disease Control and Prevention (CDC) in Atlanta, the National Institute for Communicable Diseases (NICD) in South Africa, and the World Health Organization (WHO) in Geneva. From the CDC there was Pierre Rollin, an expert on the filoviruses and their clinical impacts. Along with him from Atlanta had come Jonathan Towner, Brian Amman, and Serena Carroll. Pierre Formenty had arrived from WHO; Bob Swanepoel and Alan Kemp of the NICD had flown up from Johannesburg. All of them possessed extensive experience with Ebola and Marburg, gained variously through outbreak responses, lab research, and field studies. />

The cave served as the roosting site for about 100,000 individuals of the Egyptian fruit bat, then a prime suspect as reservoir for Marburg. The team members, wearing Tyvek suits, rubber boots, goggles, respirators, gloves, and helmets, had been shown to the shaft by miners, who as usual were clad only in shorts, T-shirts, and sandals. Guano covered the ground. The miners clapped their hands to scatter low-hanging bats as they went. The bats, panicked, came streaming out. These were sizable animals, each with a two-foot wingspan, not quite so large and hefty as some fruit bats but still daunting, especially with thousands swooshing at you in a narrow tunnel. Before he knew it, Amman had been conked in the face by a bat and taken a cut over one eyebrow. Towner got hit too. Fruit bats have long, sharp thumbnails. Later, because of the cut, Amman would get a postexposure shot against rabies, though Marburg was a more immediate concern. "Yeah," he thought, "this could be a really good place for transmission."

The cave had several shafts. The main shaft was about eight feet high. Because of all the mining activity, many of the bats had shifted their roosting preference "and went over to what we called the cobra shaft," Amman later told me. The shaft was called so because, he said, "there was a black forest cobra in there."

Or maybe a couple. It was a good dark habitat for a snake, with water and plenty of bats to eat. The miners showed Amman and Towner into the cave and led them to a chamber containing a body of brown, tepid water. Then the local fellows cleared out, leaving the scientists to explore on their own. They dropped down beside the brown lake and found that the chamber branched into three shafts, each of which seemed blocked by standing water. Peering into those shafts, they could see many more bats. The humidity was high and the temperature maybe 10 or 15 degrees hotter than outside. Their goggles fogged up. Their respirators became soggy and wouldn't pass much oxygen. They were panting and sweating, zipped into their Tyvek suits, which felt like wearing a trash bag, and by now they were becoming "a little loopy," Amman recalled. "We had to get out and cool off." It was only their first underground excursion at Kitaka. They would make several.

On a later day, the team investigated a grim, remote chamber they dubbed the Cage. It was where one of the four infected miners had been working just before he got sick. This time, Amman, Formenty, and Alan Kemp of the NICD went to the far recesses of the cave. The Cage itself could only be entered by crawling through a low gap at the base of a wall-like sliding under a garage door that hadn't quite closed. Amman is a large man, six-foot-three and 220 pounds, and for him the gap was a tight squeeze; his helmet got stuck, and he had to pull it through separately. "You come out into this sort of blind room," he said, "and the first thing you see is just hundreds of these dead bats."

They were Egyptian fruit bats, the creature of interest, left in various stages of mummification and rot. Piles of dead and liquescent bats seemed a bad sign, potentially invalidating the hypothesis that Rousettus aegyptiacus might be a reservoir host of Marburg. If these bats had died of Marburg, suspicion would shift elsewhere-to another bat or maybe a rodent or a tick or a spider? Those other suspects might have to be investigated. Ticks, for instance: There were plenty of them in crevices near the bat roosts, waiting for a chance to drink some blood.

The men went to work, collecting. They stuffed dead bats into bags. They caught a few live bats and bagged them too. Then, back down on their bellies, they squeezed out through the low gap. "It was really unnerving," Amman told me. "I'd probably never do it again. One little accident, a big rock rolls in the way, and that's it. You're trapped. Uganda is not famous for its mine rescue teams."

By the end of this field trip, the scientists had collected about 800 bats. They dissected them and took samples of blood and tissue. Those samples went back to Atlanta, where Towner participated in the laboratory efforts to find traces of Marburg virus. One year later came a paper, authored by Towner, Amman, Rollin, and their WHO and NICD colleagues, announcing some important results. Not only did the team detect antibodies against Marburg and fragments of Marburg RNA, but they also did something more difficult and compelling. They found live virus.

Working in one of the CDC's Biosafety Level 4 units (the highest level of containment security for pathogens), Towner and his coworkers had isolated viable, replicating Marburg virus from five different bats. Furthermore, the five strains of virus were genetically diverse, suggesting an extended history of viral presence and evolution within Egyptian fruit bats. That data, plus the fragmentary RNA, constituted strong evidence that the bat is a reservoir-if not the reservoir-of Marburg virus. The virus is definitely there, infecting about 5 percent of the bat population at a given time. Of the estimated 100,000 bats at Kitaka, therefore, the team could say that about 5,000 Marburg-infected bats flew out of the cave every night.

An interesting thought: 5,000 infected bats passing overhead. Where were they going? How far to the fruiting trees? Whose livestock or little gardens got shat upon as they went? The breadth of possible transmission is incalculable. And the Kitaka aggregation, Towner and his co-authors added, "is only one of many such cave populations throughout Africa."

The dangers presented by zoonoses are real and severe, but the degree of uncertainties is also high. There's not a hope in hell, for instance, as a great flu expert told me, of predicting the nature and timing of the next influenza pandemic. Too many factors vary randomly, or almost randomly, in that system. Prediction, in general, so far as all these diseases are concerned, is a tenuous proposition, more likely to yield false confidence than actionable intelligence.

But the difficulty of predicting precisely doesn't oblige us to remain blind, unprepared, and fatalistic about emerging and reemerging zoonotic diseases. The practical alternative to soothsaying, as one expert put it, is "improving the scientific basis to improve readiness." By "the scientific basis" he meant the understanding of which virus groups to watch, the field capabilities to detect spillovers in remote places before they become regional outbreaks, the organizational capacities to control outbreaks before they become pandemics, plus the laboratory tools and skills to recognize known viruses speedily, to characterize new viruses almost as fast, and to create vaccines and therapies without much delay. If we can't predict a forthcoming influenza pandemic or any other newly emergent virus, we can at least be vigilant; we can be well prepared and quick to respond; we can be ingenious and scientifically sophisticated in the forms of our response.

To a considerable degree, such things are already being done. Ambitious networks and programs have been created, by the WHO, the CDC, and other national and international agencies, to address the danger of emerging zoonotic diseases. Because of concern over the potential of "bioterrorism," even the U.S. Department of Homeland Security and the Defense Advanced Research Projects Agency (DARPA, whose motto is "Creating & Preventing Strategic Surprise") of the U.S. Department of Defense have their hands in the mix. These efforts carry names and acronyms such as the Global Outbreak Alert and Response Network (GOARN, of WHO), Prophecy (of DARPA), the Emerging Pandemic Threats program (EPT, of USAID), and the Special Pathogens Branch (SPB, of the CDC), all of which sound like programmatic boilerplate but which harbor some dedicated people working in field sites where spillovers happen and secure labs where new pathogens can be quickly studied. Private organizations such as EcoHealth Alliance (led by a former parasitologist named Peter Daszak) have also tackled the problem. "You come to this blind room and the first thing you see is just hundreds of these dead bats."There is an intriguing organization called Global Viral (GV), created by a scientist named Nathan Wolfe [who won a Popular Science Brilliant Ten award in 2005], and financed in part by Google. GV gathers blood samples on small patches of filter paper from bush-meat hunters and other people across tropical Africa and Asia and screens those samples for new viruses, in a systematic effort to detect spillovers and stop the next pandemic before it begins to spread. At the Mailman School of Public Health, part of Columbia University, researchers in Ian Lipkin's laboratory are developing new molecular diagnostic tools. Lipkin, trained as a physician as well as a molecular biologist, calls his métier "pathogen discovery" and uses techniques such as high-throughput sequencing (which can sequence thousands of DNA samples quickly and cheaply), MassTag-PCR (identifying amplified genome segments by mass spectrometry), and the GreeneChip diagnostic system, which can simultaneously screen for thousands of different pathogens. When a field biologist takes serum from flying foxes in Bangladesh or bleeds little bats in southern China, some of those samples go straight to Lipkin.

These scientists are on alert. They are our sentries. They watch the boundaries across which pathogens spill. When the next novel virus makes its way from a chimpanzee, a bat, a mouse, a duck, or a macaque into a human, and maybe from that human into another human, and thereupon begins causing a small cluster of lethal illnesses, they will see it-we hope they will, anyway-and raise the alarm.

During the early 20th century, disease scientists from the Rockefeller Foundation and other institutions conceived the ambitious goal of eradicating some infectious diseases entirely. They tried hard with yellow fever, spending millions of dollars and many years of effort, and failed. They tried with malaria and failed. They tried later with smallpox and succeeded. Why? The differences among those three diseases are many and complex, but probably the most crucial one is that smallpox resided neither in a reservoir host nor in a vector, such as a mosquito or tick. Its ecology was simple. It existed in humans-in humans only-and was therefore much easier to eradicate. The campaign to eradicate polio, begun in 1998 by WHO and other institutions, is a realistic effort for the same reason: Polio isn't zoonotic. Eradicating a zoonotic disease, whether a directly transmitted one like Ebola or an insect-vectored one such as yellow fever, is much more complicated. Do you exterminate the pathogen by exterminating the species of bat or primate or mosquito in which it resides? Not easily, you don't, and not without raising an outcry. The notion of eradicating chimpanzees as a step toward preventing the future spillover of another HIV would provoke a deep and bitter discussion, to put it mildly.

That's the salubrious thing about zoonotic diseases: They remind us, as St. Francis did, that we humans are inseparable from the natural world. In fact, there is no "natural world," it's a bad and artificial phrase. There is only the world. Humankind is part of that world, as are the ebolaviruses, as are the influenzas and the HIVs, as are Marburg and Nipah and SARS, as are chimpanzees and palm civets and Egyptian fruit bats, as is the next murderous virus-the one we haven't yet detected. And while humans don't evolve nearly as fast and as variously as an RNA virus does, we may-let me repeat that word, may-be able to keep such threats at bay, fighting them off, forestalling the more cataclysmic of the dire scenarios they present, for one reason: At our best, we're smarter than they are.

David Quammen lives in Bozeman, Montana, and can be found on Twitter, @DavidQuammen. His book, Spillover, is available this month

"Our robot, named Achilles, is the first to walk in a biologically accurate way. That means it doesn't just move like a person, but also sends commands to the legs like the human nervous system does.

Each leg has eight muscles-Kevlar straps attached to a motor on one end and to the plastic skeleton on the other. As the motor turns, it pulls the strap, mimicking the way our muscles contract. Some of Achilles' muscles extend from the hip or thigh to the lower leg so they can project forces all the way down the limb. This allows us to put most of the motors in the hips and thighs. Placing them up high keeps the lower leg light, so that it can swing quickly like a human's lower leg.

In people, neurons in the spinal column send out rhythmic signals that control our legs. It's like a metronome, and sensory feedback from the legs alters the pace. Your brain can step in to make corrections, but it doesn't explicitly control every muscle, which is essentially why you can walk without thinking about it. For our robot, a computer program running off an external PC controls movement in a similar way. With each step, the computer sends a signal to flex one hip muscle and extend the other. The computer changes the timing of those signals based on feedback from the legs' load and angle sensors. A similar control system handles the lower muscles.

Modeling human movement has applications outside of robotics. It could also help us understand how people recover after spinal-cord injuries, for example. But our robot is still a very simplified model-it has no torso and can't handle complex terrain. Initially, we also had a problem with its feet slipping. We thought about different types of rubber to give its feet more grip but eventually realized a solution already exists. Now, the robot wears a pair of Keds."

-Theresa Klein, an engineer at Orbital Sciences Corporation, created Achilles while she was a graduate student at the University of Arizona

Walking on the surface of Titan would be like walking on a beach while the tide is going out, according to a new study. Or, if snow is your preferred outdoor surface, it's like breaking a snowshoe trail on a sunny day. The huge Saturnian moon's surface has the consistency of damp sand or crusty snow--you can walk gently on top, but push hard with your foot and you'll break through, sinking down at least a few inches.

This comes from a new analysis of what happened to the Huygens lander, an oft-forgotten component of the Cassini-Huygens mission to the Saturn system. Huygens was a 400-pound lander that apparently "bounced, slid and wobbled" until coming to rest on the surface of Titan. Previous analysis of its fate suggested that Titan had a soft surface, but now NASA knows it's more complicated than that. Touch it lightly and it seems hard, but with more pressure, it yields.

Huygens parachuted to the surface of the moon and made a dent 4.7 inches deep before bouncing out onto a flat surface, according to NASA. It didn't splat, which it would have done if the surface was muddy with liquid methane. This suggests it hadn't rained any methane or ethane in a while when the probe landed. Huygens hit the ground with an impact speed similar to dropping a ball on Earth from a height of 3 feet, according to NASA.

The study analyzed data from Huygens, computer simulations and Earth-bound drop tests. It's published in the journal Planetary and Space Science.

[JPL]

As if Felix Baumgartner's supersonic skydive didn't have enough built-in tension, his ascent to 128,100 feet on Sunday morning was plagued by an unexpected complication: a problem with his faceplate. Anyone listening to the live feed on Sunday would have heard Felix tell mission control that he didn't think he had sufficient heat-and then the conversation between Felix and mission control abruptly ended. Joe Kittinger uttered a code word that cued the broadcast trucks to cut the feed. So what exactly happened?

In short: They nearly aborted the mission. As he ascended up through 80,000 feet, Felix indicated that he wasn't feeling the faceplate heating system kick in properly. When Felix exited the capsule, he would be falling through temperatures as low as minus 60 degrees Fahrenheit. And he needs to see the horizon in order to maneuver into a stable position.

"The worst thing that can happen to a guy is a faceplate that doesn't work," Kittinger says now. "Heat is required to keep that faceplate from freezing over. Think about this: He has no idea where he is, no visible help; he's just a bomb that's falling through the air that can spin and tumble violently. The only way he knows what altitude he's at is when pressure suit deflates at 35,000 feet. Because he's blind, absolutely blind."

If he can't see his wrist altimeter, Felix has been trained to count to 60 after he feels his suit depressurize and then pull his parachute; that's when he'll be in an environment with enough oxygen to breathe (there's only 10 minute worth in his bailout bottles). But if he had blacked out- as Kittinger had on his first Project Excelsior jump-and if for some reason his automatic chute opener didn't go off, he could impact the ground.

"If you start talking about that problem when you're out on that step," Felix says, it's too late. "I'm already released from ship's system, and that means I only have 10 minutes of oxygen. You better know what you want to do way before that. I have to put it in my memory because you cannot think and come up with decisions while you freefall. It's just too fast and too overwhelming."

Art Thompson, the project's technical director, quickly gathered his team in mission control, including two representatives of the David Clark Company, which built Felix's suit. The faceplate heating system is powered by the capsule on the way up and by a battery in Felix's chest pack on the way down. That's one of the innovations to this spacesuit. U-2 pilots actually eject in their seats, kicking out of them only when they descend to 15,500 feet; the seat contains the battery pack that heats the pilot's faceplate, says Dan McCarter from David Clark. The Stratos team needed to figure out the source of Felix's problem: Was it the visor itself or the capsule's electrical system? Or a third possibility: his visor wasn't frosting, but simply fogging up as he exhaled?

"We came up with the plan to disconnect from the capsule system and go on the chest pack to verify that the system could go to full heat," Thompson says. But that meant also disconnecting from the capsule communications system-and because Felix's radio antennas are on his legs, and he was still sitting in a fully pressurized capsule, they didn't know if they would be able to reconnect with him. As it turned out, the visor worked, and they were able to communicate. But by now they were at roughly 112,000 feet.

Mission control presented Felix with options, which included riding the capsule back down under its recovery parachute; it would be a rough landing but a survivable one. "We talked back and forth and we finally came up with a solution," Felix says. If he stepped out of the capsule and his visor began to freeze, he could release his drogue chute after 30 seconds of falling, which should stabilize any uncontrolled spinning and safely deliver him to 35,000 feet still conscious.

It was a calculated risk he was willing to take. "It's a team decision but at the very end I have to make that call because it's my life," he says.

Teenagers take more risks than younger children and adults, a fact that is borne out by statistics and just plain obviousness. But why? It's not because they all have an obsession with danger--they are more willing to accept risks, even when they don't know what will happen, according to a new study.

Yale researchers asked 65 people, who ranged in age from 12 to 50, to make some decisions in a fake lottery, each with different degrees of risk. Sometimes their odds of winning were clear, but sometimes they were ambiguous, so the participants couldn't be sure how likely they were to win. When the risk was precisely stated, adolescents were just as likely to avoid them as anyone. But when risks were unclear, they were more OK with them than other age groups. Ifat Levy, assistant professor in comparative medicine and neurobiology at Yale, said this makes sense because "Young organisms need to be open to the unknown in order to gain information about their world."

Because of this, young organisms of the human kind are also more likely to get hurt and to die. The injury and death rate for adolescents is 200 percent greater than it is for younger kids, according to this study. It appeared in the Proceedings of the National Academy of Sciences earlier this month.

[Yale News]