Australian tree frog.

Photo by Stephen Barnett on Flickr, licensed under Creative Commons

Frogs can jump pretty far, right? The general image of a frog is one with a lithe torso and long back legs to give it that necessary lift. But depending on where they tend to live (in trees, in water, or burrowed underground) the little amphibians can actually have very different styles of jumping. For example, tree-dwellers can leap to great heights, but only across short distances. Burrowing frogs have shorter legs and rounder, squatter bodies, resulting in rather small hops (which, though unimpressive, are much more suited to their needs than high jumps would be). Marta Vidal-García, a PhD student at the Australian National University, has previously studied the role evolution and environment play in shaping frogs' bodies, and is now investigating how habitat and body shape affect the way different frog species move. In her most recent research, presented at the Annual Meeting of the Society for Experimental Biology, she used two high-speed cameras to film about 230 wild frogs from about 30 different species, then had a computer program analyze the footage to determine each jump's height, distance, and speed. 

Flooding near Council Bluffs, Iowa, on June 16, 2011.

US Army Corps of Engineers

The data was collected by twin satellites, from NASA's Gravity Recovery & Climate Experiment (GRACE) mission, which can measure water on the surface of the Earth. The model uses this information to predict how much of that water will flow into the river valley in the future, and hence whether flooding is likely. "Just like a bucket can only hold so much water, the same concept applies to river basins," study lead author J.T. Reager, an earth scientist at the University of California, Irvine, told LiveScience.

But there are reasons not to get overly excited at this instant. For one, the model has to date only been used to analyze past floods, although the researchers hope to apply it to future scenarios. There is also currently a three-month lag time to get the data from the GRACE satellites, meaning that we can only make predictions for about two months in the future, which is about the same warning time given with current practices (although NASA is working to get GRACE data within 15 days of collection in the future, LiveScience noted). The method also cannot predict flash floods from rapid downpours. 

Furthermore, people don't always listen. The National Weather Service, for example, starting warning people about impending Missour-river flooding in April (though this almost certainly saved lives, according to the agency). A more intractable problem is the enormous amount of buildings, towns, roads and other infrastructure built on the flood plains of the Missouri, the Mississippi, and rivers around the world--which by definition, occasionally flood.

The massive amount of water stored in the Northern Plains and Rocky Mountain regions, from snowfall and rain during the wet winter of 2010-2011, can be seen in blue.

Nature Geoscience

Image of Saturn Taken by Cassini, April 2, 2014

NASA/JPL-Caltech/Space Science Institute

Like a photo of the New York City skyline with both the Empire State and Chrysler buildings in view, this image of Saturn shows off its most iconic landmarks. There's the hexagon-shaped jet stream feature at its north pole, plus its rings. The spacecraft Cassini took this image on April 2.

Cassini recently celebrated the tenth anniversary of its arrival at Saturn. Now, its engineers are looking toward its final missions. In 2015, NASA plans to send Cassini to sample the water geysering out of Saturn's moon Enceladus. This will be humanity's first and only sample of that alien water. Then, in late 2016, Cassini will begin a series of 22 orbits around Saturn that will send the spacecraft between Saturn's upper atmosphere and its innermost rings. Such close encounters with the planet will help scientists measure Saturn's magnetic field and the mass of Saturn's rings—another first.

The 22 orbits Cassini will make around Saturn in its final mission

NASA/JPL-Caltech

Finally, Cassini will plunge into Saturn's atmosphere to avoid contaminating the planet's moons, which scientists think may harbor alien life.

A species of stingless bee (Trigona spinipes), also known as arapuá, examined in the study.

José Reynaldo da Fonseca via Wikimedia Commons

Imagine you're a bee. Buzz, buzz, you're looking for flowers. Good for you. Now, as you might imagine, there are competing bees afoot--naturally you're not the only species looking for pollen and nectar. Let's say you've found a nice cluster of flowers, a good source of food. You might imagine that with competing bees--eavesdroppers--around, it is best to communicate quietly. In many cases, you would be right. But that's not always true. Sometimes it is best to conspicuously communicate the location of a food source to your friends, eavesdroppers be damned!

A new study found that in the presence of competitors, several species of stingless bees make a big stink about the location of their food (somewhat literally: the bees signal its location with loads of smelly pheromones). Perhaps counterintuitively, they found, this actually helped both themselves and their competitors, for this reason: When one species finds a good food source or flower, they tend to defend it heavily against other bees. So by making their flower-claim clear, the species signals that they have found it, and are willing to defend it. This allows the other species to steer clear, and avoid putting up all the energy that would be required for stealing away said flower.

On the other hand, food sources with fewer pheromones were readily visited by competing bees. 

“Until now, it was thought that eavesdroppers select against conspicuous signals, for example by more easily finding and eating prey that sings loudly," said Washington State University researcher Elinor Lichtenberg, a co-author of the study, which was published this week in Current Biology. "But our results show that eavesdroppers can help select for the same conspicuous signals that are easiest for intended recipients to detect and understand.” 

The finding shows that eavesdroppers can affect the evolution of animal communication in unexpected ways--sometimes dampening a signal, sometimes amplifying it.

Many species of stingless bees, by the way, also produce honey, and the craft of rearing and producing the sugary treat from these animals is an ancient one (called meliponiculture), practiced for example by the Maya to this day.

Signs like this were used to show which houses had received the smallpox vaccine

PAHO

Surprise! While preparing to move to a new lab, scientists at the U.S. National Institutes of Health discovered something unexpected in the old one: little vials containing smallpox virus. By international agreement, samples of smallpox are only supposed to be kept in one of two labs in the world. One is part of the U.S. Centers for Disease Control and Prevention in Atlanta. The other is the VECTOR Institute in Russia.

There's no evidence that anyone has taken or used the vials, according to a statement from the Centers for Disease Control and Prevention. In addition, biosafety staff at the NIH don't think there's any risk that anybody got sick from the vials. The CDC believes the vials may date from 1950s, when many labs held smallpox for research. But the centers' Division of Select Agents and Toxins is still investigating who prepared the samples and how they ended up in this unused NIH freezer.

The surprise vials were labeled "variola," the scientific name for smallpox, ABC News reports. A number of other vials in the same freezer weren't labeled at all. When NIH scientists first discovered the vials on July 1, they secured them and alerted the CDC, which sent three experts to come pick the virus up in a government plane. Tests confirmed the six labeled vials contained smallpox DNA, while the other vials didn't.

The CDC plans to perform further tests to see whether the virus in the vials is "alive" enough to grow in petri dishes in lab. After that, it plans to destroy the viruses. 

Vaccination campaigns eradicated smallpox from the world in 1979. That same year, labs around the world agreed to either destroy their own variola samples or to send them to one of the two approved labs. As far as officials could tell at the time, all stockpiles outside of the CDC and the VECTOR Institute were gone by the early 1980s.

Most people now don't even get vaccinated against the disease. Only researchers who work on smallpox, certain healthcare workers, and other people who are at high risk get the vaccine, because it has some rare but potentially deadly side effects; balance that against the fact that smallpox has been eradicated in the wild, and no organization recommends routine vacciation.  Governments do often hold stockpiles of the vaccine, which doesn't contain variola itself, so it doesn't break the international agreement. There's no cure for smallpox, which can kill from 30 percent to nearly all those who contract it.

[ABC News, Centers for Disease Control and Prevention]

Soccer Exoskeleton

Juliano Pinto, a paraplegic man, kicks a soccer ball using an exoskeleton built by Miguel Nicolelis and a large team of scientists and engineers.

Imagine Science Films

The World Cup has drawn more than rabid soccer fans to Brazil. A team of filmmakers are on the ground in Rio de Janeiro documenting the science behind the games, including an exoskeletal kick-off, the genetics of competition, and even the biochemistry of diehard spectators.

Here's Imagine Science Films' take on Kinetic, the latest mini-documentary in their "Field Work: World Cup" series:

Imagine Science Films teams up with Miguel Nicolelis, Director of the Institute of Neurosciences in Natal to discuss the neurobiology of translating thought into mechanical action in Kinetic.

What if you could move technology simply by imagining it? If this sounds like a science fiction movie, rest assured, it is all too real. The exoskeletal kick off of the World Cup, performed by Juliano Pinto who lost motor control of his lower body in a car accident, left many of us wondering, how did he do it?

Movement does not stem from one part of the brain, but neurons from many parts of the brain work in tandem to complete actions.

“Think of the brain as a big democracy,” says Miguel Nicolelis, who led a team of researchers to create the robotic exoskeleton used to prompt muscle movement. “Lots of cells ‘vote’ electrically to produce this behavior from different parts of the brain.”

The more neurons that join in, the better.

The sensors placed on Juliano Pinto record angle, position, pressure, and temperature, that is then fed back to the subject through vibrations placed on their torso. These vibrations create an illusion in the brain itself that the subject is responsible for limb movement. In a sense, the exoskeleton is incorporated as an extension of the person’s body.

Watch the film below.

Not working? Watch Kinetic on YouTube.

This article was created in partnership with Imagine Science Films. Watch all of the Field Work videos here.

Super Typhoon Neoguri

2014's first Pacific megastorm hit Okinawa, Japan on the morning (local time) of July 8.

NASA/GSFC/Jeff Schmaltz/MODIS Land Rapid Response

The storm became so powerful as it neared the island chain that officials urged around a half-million of the prefecture's 1.4 million residents to evacuate to safer ground. When Neoguri hit it was Category 3, slightly subdued from its peak strength, but still with torrential rains and battering winds: The U.S. military's Kadena Air Base on Okinawa Island measured sustained winds of up to 74 miles per hour, and gusts peaking at 101 mph, while the Japan Meteorological Agency (JMA) recorded 79 mph and 118 mph respectively on nearby Tokashiki Island, according to The Weather Channel (TWC), as well as about 9 inches of rainfall. TWC also states that according to local media, the storm is responsible for 1 death and 25 injuries.

Now Neoguri headed for mainland Japan, as this tracking image from the JMA shows:

Typhoon Neoguri's preditcted track across Japan.

Japan Meteorological Agency

As the storm sweeps east-northeast across Japan's main island over the next few days it is expected to weaken, with winds of around 50 mph by the time it get to the northernmost Tohoku region early on Friday.

Neoguri, by the way, apparently translates as "raccoon dog," the English name for a group of canids native to East Asia. Neoguri are related to wolves, domesticated dogs, foxes, and other canids...but not raccoons, which hail from a different evolutionary tree despite the similar mask patterns on their faces.

Tanuki, a native East Asia canid

663highland/Wikimedia Commons

A subspecies of neoguri native to Japan called tanuki, also a small masked canid, is a mainstay of Japanese folktales as a mischevious shapeshifter. Tanuki show up in contemporary pop culture too -- like Seijun Suzuki's eye-poppingly weird and wonderful 2005 fantasy movie "Princess Raccoon":

George Washington Bridge, New York, 2003

Bob Jagendorf

Very early in the morning on Monday, officers with the New York Police Department arrested two men for flying a drone near the George Washington Bridge. The officers were dispatched by an NYPD helicopter pilot, who claimed the drone came within 800 feet of his chopper. Nestled within this sparseness is everything frustrating about the state of drone regulation today.

Drone law is murky on this matter. The Federal Aviation Administration is the agency responsible for integrating drones into skies with manned aircraft, but so far they've taken a very gradual approach. The goal is to balance the future needs of industry, the present-day habits of hobbyists, with an overriding concern for the safety of vehicles with people on board. Small drone use is restricted to non-commercial activity, and pilots are supposed to adhere to model airplane rules. The FAA guidelines say model airplanes are not supposed to fly higher than 400 feet. It also says they should avoid flying near manned aircraft, but leaves "near" undefined.

A further update to these rules, published in June, offers broader guidance for drone pilots but also muddies what, exactly, is a legal way to use drones. A chart delineating legal hobbyist uses from illegal ones relies heavily on how drone photography is used after a flight. In a report on FAA progress, the Inspector General emphasized the problems caused by murky interpretations of flight rules.

Fortunately for the FAA, at least, police in this case won't need to rely on specific drone rules when arguing that the flight was illegal. The most salient argument is that flying a drone close to another aerial vehicle on its own qualifies as reckless endangerment under New York law. As with all matter of court, there may be evidence that weakens this claim. 

This isn't the first time local law in New York has faced a case of drones and risk. In September 2013, when a young man was partially (and fatally) decapitated by the drone he was flying, New York police investigated the scene of the accident.

An Implantable Microchip for Delivering Drugs

These images are from 2012, when MicroCHIPS published a paper on using an implanted device to deliver daily doses of an osteoporosis drug.

Courtesy of MicroCHIPS, Inc., Massachusetts

It's a whole new level of set it and forget it. Researchers are testing a remote-controlled implant that releases daily doses of hormonal birth control into the body, MIT Technology Review reports. The implant is designed to last up to 16 years.

If and when the user wants to conceive, she simply clicks the implant's remote control to turn it off. When she wants to prevent pregnancy again, she can click to restart the minute machine.

The implant's developer, MicroCHIPS of Massachusetts, is now testing its little chip in animals. The implant has been previously tested in people for four months, for delivering daily osteoporosis medicine. If the new birth-control tests go well, MicroCHIPS will have to test the chip-and-hormone package in people. At that point, the company will have to verify things like the chip's failure rates and how safe it is to keep in the body for an extended period of time. That means years of work. Ensuring that a product that worked in lab animals also works in people is a tough challenge for any medical device, but we're rooting for this one.

The coolest thing about the chip is its release mechanism. MIT Technology Review reports:

There's lots more to learn there. In addition, the BBC reports that MicroCHIPS hopes to make the implant available to women around the world who don't have good access to birth control today.

[MIT Technology Review, BBC]

New molecules that chop up DNA may fight deadly diseases.

Stew Dean via Flickr CC

Jay Johnson was part of a clinical trial testing a radical technology that precisely cuts and modifies DNA that may cure his HIV. The new treatment is being tested on diseases long thought to be beyond the reach of genetic therapies, including HIV, brain cancer, and Alzheimer’s disease. Inspired by nature and engineered by researchers, scientists have discovered three classes of proteins that cut and paste DNA, all known by their somewhat cumbersome acronyms: ZFNs, TALENs and CRISPRs.

ZFNs: Zinc Finger Nucleases

When exploring the genetic code of the African clawed frog, scientists noted an odd protein tightly bound to the frog’s DNA. When they mapped the 3D architecture of the protein, they were surprised to see elongated loops resembling fingers, grasping the frog’s genes with extraordinary strength. Holding the loops together was a stable zinc ion. Because of its unusual hand-like structure, they named the protein zinc finger.

A decade later Srinivasan Chandrasegaran, then a postdoctoral fellow at Johns Hopkins, wondered how he could make practical use of the sticky proteins. The problem was that each zinc finger recognized only a tiny chunk of DNA, about three bases. This kept the collection from being specific enough to target genes in people. If he wanted to use the proteins to target a specific piece of DNA, he needed more length. Chandra, as his friends called him, had a simple solution. He stitched six of the proteins together so that instead of just three bases, he had eighteen, enough to recognize a fragment of a gene.

But binding the DNA wasn’t enough. He also had to figure out a way to alter it. Chandra decided to borrow an enzyme used by bacteria to cut out viruses from their genetic code. Called restriction endonucleases, this clever defense mechanism is an ideal way to cut DNA. Chandra chose the FokI restriction enzyme, known for its ability to make a clean break. Chandra combined the DNA gripping ability of the zinc fingers with the DNA cutting enzyme. A zinc finger nuclease (ZFN) was born.

To make the technology safe in humans, two ZFNs are delivered directly to the nucleus of the cell, where they bind to two separate pieces of DNA surrounding their genetic ‘prey.’ Then the cutting enzymes dimerize, locking onto each other. Only after they’re locked together can the enzymes engage, snipping through the DNA. The cell has trouble repairing this kind of double-stranded break, so the end result is a mangled and dysfunctional gene. A similar process can be used to repair a gene instead of breaking it, allowing genetic material to be inserted into the cell. In a major breakthrough, scientists using this method can now target just about any gene.

A small California biotech, Sangamo Biosciences, has developed ZFNs commercially. Sangamo is currently conducting clinical trials for therapies for everything from HIV to hemophilia to Alzheimer’s disease.

Breakthroughs seem imminent. In March, an article published in the New England Journal of Medicine reported results from a Phase II clinical trial for HIV. This trial treated HIV by cutting the CCR5 gene. CCR5 is kind of like an appendix--it's not necessary for human health. On the other hand, it’s vital for HIV. The vast majority of HIV strains need the CCR5 receptor to enter human cells. Thanks to a mutation called Δ32, people with a defective gene are resistant to the virus, which is another reason why Sangamo hopes they can treat HIV by carving up the gene. Their study found that in the 12 people tested, the technology is safe. It’s still very early, but the data is promising, showing a rise in cells modified by the ZFNs corresponding to a decrease in HIV. Jay Johnson is one of the 12 receiving this cutting edge therapy in hopes of curing his HIV.

TALENs: Transcriptor Activator-Like Effector Nucleases

While ZFNs came from a small, aquatic frog, TALENs were adapted from bacteria, specifically a plant pathogen named Xanthomomas, which preys upon the plant’s genetic code.

Feng Zhang was a graduate student at MIT and frustrated by the complexity of genome modification. Because ZFNs grasp DNA with their finger-like elongations, they are difficult to design and expensive to produce. To get around this problem, Zhang turned to TALENs.

There are no finger-like structures in these proteins. Instead the DNA binding is reminiscent of how it occurs naturally in our cells. The amino acids that make up the TALEN precisely align with the DNA sequences they cut. Changing the amino acids in the TALEN changes which sequences it binds to, making customized alterations of the proteins far simpler. Even better, each TALEN recognizes 17 bases of DNA, plenty long enough to recognize a piece of human DNA. That’s part of the reason TALENs have taken the lead from ZFNs.

TALENs use the same FokI enzyme that cuts through DNA in ZFNs, which makes it relatively easy to design a TALEN capable of specifically binding human DNA. In both processes, two binding agents flank the gene and then move in, the enzyme creating a double-stranded break the cell can’t recover from.

While ZFNs have been around for a decade, TALENs are relatively new. They don’t have the rigorous safety testing available in humans ZFNs do. But while the research is ongoing, where TALENs have proven useful is in disease modeling. Scientists have created disease cell lines, identical except for a single TALEN-created mutation. It’s an ideal system for reverse genetics, tracing a lone genetic mutation to its effect in the cell. Disease models have now been made for hepatitis C, blood cholesterol levels, insulin sensitivity, and others. TALENs are effective at genome editing, and because of their innate simplicity, may can be used in humans.

CRISPRs: Clustered Regularly Interspaced Short Palindromic Repeats

The newest kids on the DNA chopping block are CRISPRs. Like TALENs, CRISPRs arise from bacterial defenses against viruses. They are are small repeating palindromes spaced throughout the bacterial genome. In between these repeating sequences are “guides,” small chunks of genetic code that match those of the invaders. They lead the CRISPR to the right spot in the DNA. With their help, the CRISPRs bind to the target DNA, forming a tight structure with the intruder's genetic code. Instead of using the FokI nuclease like ZFNs and TALENs, CRISPRs use Cas9, a similar bacterial enzyme, capable of making deep cuts in DNA. But the effect of the enzyme is the same: because it creates a double-stranded break, the cell can’t repair it. Just like with ZFNs and TALENs, the gene is taken out of commission. (Also like ZFNs and TALENs, DNA can be added at the cut site to potentially repair a gene.)

Of the three, CRISPRs have the most elegant design. There’s no need for complicated protein structure here, just clean lines of genetic code tied to the cutting enzyme. The simplicity creates a streamlined cell delivery, which is a big advantage. Yet in some ways, the sheer simplicity is frightening. The system doesn’t have the same safeguards that prevent against off-target effects, like if the protein goes rogue and potentially cuts at an unintended site.

Feng Zhang has been at the forefront of CRISPR development, rapidly producing mutant cell lines and mouse models. In just one year, researchers have used CRISPRs to target genes in models of cystic fibrosis, sickle cell anemia, and autism. While developing animal models of disease used to take months and even years, it’s now being done in weeks.

CRISPR technology is moving ahead at lightning speed. This February, scientists in China published their study of CRISPRs in monkey embryos. They targeted physiological genes involved in development. The two infant primates are now under close observation. Remarkably, the researchers were able to alter two genes in a single step. Despite the worries of off-target effects, none have been observed. Instead, other fears have been raised. Some groups are concerned that this technology is likely to expand the role of animal testing. One thing is certain: With the use of CRISPRs in primate models, the technology is inching closer to use in humans.

The potential of CRISPRs is clear in a recent Nature Biotechnology study. Researchers at MIT used the technology to correct a mutation in the FAH gene in a mouse model of a rare human genetic disorder called tyrosinemia. The disorder causes an excess of the amino acid tyrosine, which can lead to liver failure and even death. Humans with the disease take a drug to control the production of the amino acid. In the mouse model, animals with the disorder controlled the disease with the same drug. But after CRISPRs were delivered to the animals, the modified cells proliferated, eventually making up one-third of all the animals’ liver cells and ultimately curing the three mice tested.

Genomic surgery has the potential to treat an incredible variety of human disease. But along with this potential comes concerns, both ethical and scientific, of forever altering a person’s DNA.

Back at the University of Pennsylvania hospital, Jay Johnson was optimistic as the needle pricked into his vein to deliver his own chopped up DNA back into his bloodstream. It took only a few minutes for the ZFN treated cells to be infused into his body. Ten minutes later he started to feel extremely cold. Twenty minutes later the cramping began. He felt like his “whole body was a big ball of knots.” Jay Johnson was the only person in the group of twelve to experience an adverse reaction. His experience is an important reminder that these techniques are not just about the conceptual beauty and function of DNA-cutting proteins. When put into practice, the techniques are being used on  people—who by necessity are guinea pigs for the emerging technology.

Still, despite his adverse reaction, Jay Johnson is healthy and would gladly sign up for another clinical trial. He’s not fearful of the technique, only hopeful for the potential benefits. His participation in research is, he says, “Not only for myself, but for science.”

The most "beautiful" route between two points in Boston on the left. The quickest route, on the right.

Quercia et al

If you want to find the most scenic route to get somewhere, there may soon be an app for that. Daniele Quercia and colleagues at Yahoo Labs in Barcelona have come up with a way to create a crowd-sourced measure of a city's beauty, and made an algorithm to find the prettiest way to get from one point to another. "The goal of this work is to automatically suggest routes that are not only short but also emotionally pleasant," the scientists told Technology Review:

Quercia et al then got 30 actual human beings in London and another 54 in Boston to test out this internet-collected data, and the subjects agreed that the more beautiful areas--according to the program--were indeed more beautiful. 

To add power to the algorithm, the team mined data from photos with GPS tags posted to Flickr, taking into account "positive emotions" ascribed to different locations, and also computing how many photos were taken in different places (not many people take photos of really drab or mediocre sites, as you might expect). They are currently working on a mobile app, to test in different cities in Europe and the U.S. Until then, you could just ask a real breathing resident what route they would suggest--but that would involve human interaction.

[Tech Review / arXiv]

A ubiquitous type of bacteria may be the source of much of the ocean's methane.

Ah, the oxygen-rich surface of the ocean, where the air and water meet, and life flourishes. But you might not know that these waters are also supersaturated with methane relative to the atmosphere, a phenomenon termed the "marine methane paradox." The question being: Where does this methane come from? The answer matters because this methane eventually makes its way into the atmosphere, where it readily traps heat, giving it a 20-fold greater impact on climate change than carbon dioxide, pound for pound. 

It was previously thought that methane could only be produced by bacteria in anaerobic, or oxygen-devoid environments. So what's going on here? 

It turns out the culprit may have been hiding in plain sight all along, so to speak. New research suggest much of the methane is produced by the most abundant organism in the ocean, a group of very simple and tiny bacteria called SAR11. Usually these bacteria don't produce methane, but the study, published in Nature Communications, shows that they can produce the gas as a byproduct of their natural metabolism when they are starved for phosphorus. 

The microbes make the methane from a substance called methylphosphonic acid, which is in turn excreted by another type of Archaebacteria. This acid contains phosphorus, and when the element becomes scarce (as it does in various parts of the ocean, often on a seasonal basis, for a variety of reasons) the SAR11 microbes digest the acid, releasing methane. The exact amount of methane produced this way is unknown. In terms of remediation, for now it makes more sense to address human-associated sources of methane, like mining, fracking, and cattle. 

“Their ability to [produce] methane is an interesting finding because it provides a partial explanation for why methane is so abundant in the high-oxygen waters of the mid-ocean regions,” said study co-author and Oregon State University microbiologist Steve Giovannoni, in a statement. “Just how much they contribute to the methane budget still needs to be determined.” But the results could help fill in scientists' understanding of the carbon cycle, which could possibly help create more accurate climate models.

On December 5, 2011, Andrew Meas wiggled his toes for the first time since a motorcycle accident four years earlier paralyzed him from the chest down. Within a week, he was beginning to stand. Meas’s remarkable (albeit partial) recovery comes courtesy of a groundbreaking use of an electrode array implanted over his spinal cord. 

For decades, researchers have been seeking ways to help the millions of people with spinal cord injuries regain control of their limbs, with frustratingly little success. The new device provides a rare glimmer of hope. Scientists at the University of Louisville’s Kentucky Spinal Cord Injury Research Center, where Meas and three other patients received their im­plants, speculate that the stimu­lation may be reawakening connections between the brain and the body. “There’s residual circuitry that we can recover that no one realized was possible to do,” says Reggie Edgerton, director of the Neuromuscular Research Laboratory at the University of California, Los Angeles. “We were shocked.” 

Some of the benefits, such as better bowel and bladder control and improved blood pressure, remain even when the device is switched off. Electrical stimulation isn’t a cure, of course. The patients still can’t walk. And the stimulation must be customized for each individual, a time-consuming process. But it’s an enormous advance nonetheless. Says Edgerton, “It opens up a whole new mechanism of recovery.” 

Illustration by Son of Alan

A) When a person with a spinal cord injury thinks about wiggling his toes, the message travels from the brain down the spinal cord, but fails to reach its destination. 

B) An array of 16 electrodes implanted over the lower spinal cord stimulates circuitry that controls the lower body, awakening dormant neurons that carry the message.

C) A wire connects the electrode array to the stimulator, a rechargeable device about the size of a pager, implanted in the abdomen just below the skin. 

D) The stimulator contains programs that excite various neural circuits. Different frequencies, voltages, and combinations of electrodes enable different movements. 

E) A handheld remote allows the user to select which circuits he wants to stimulate—for example, left toes or right leg. 

This article originally appeared in the July 2014 issue of Popular Science.

Fish on wheels

Photograph by Studio diip

If Thomas de Wolf gets his way, pet fish will soon navigate terra firma. A co-founder of Netherlands design firm Studio diip, de Wolf built a motorized tank that empowers goldfish to drive around. “We wanted to make something that showcases computer vision technology, but not in such an industrial way,” he says. “We thought, ‘Let’s do something for fish.’ ” De Wolf and fellow industrial designer Guust Hilte built a platform to hold a one-gallon tank and attached four DC motor–powered wheels, a miniature computer, and a battery pack. A webcam monitors the tank from above, and software analyzes the image feed to determine where the fish is. Then the program steers the tank relative to the fish’s location* (e.g., if it’s at the front of the tank, the tank moves forward). The fish-on-wheels may yet graduate from a laboratory one-off; de Wolf launched a crowdfunding campaign to try to bring a consumer-friendly device to market.

Time: 1-2 weeks

Cost: $550

The tank’s computer-vision software is designed to work with goldfish. It tracks orange pixels and translates them into steering instructions.

Photograph by Studio diip

*De Wolf says no fish were harmed during the creation of his tank.

Watch the fish drive de Wolf's tank below:

This article originally appeared in the July 2014 issue of Popular Science.

The Guinea Worm. Creepy, but still here... for now.

Coastal Courier

The guinea worm is one seriously disturbing parasite. When someone ingests its larvae by drinking unfiltered water, the worm reproduces and incubates for months in the person's abdomen, sometimes growing up to three feet long. Eventually it slithers out through an excruciating sore on the person’s leg or foot, but it takes it's time in leaving--sometimes up to several weeks. The guinea worm has afflicted humans across central Africa and Southeast Asia for millennia, relying on us for its proliferation.

Thanks to public health efforts from organizations like the UNICEF, World Health Organization and The Carter Center, the cycle might end altogether. For the last 30 years the organizations have been mapping cases the disease, implementing awareness programs and safe containment strategies, and ensuring access to clean water for those at risk. Their efforts have paid off; this week, the Carter Center announced that the number of cases of guinea worm reported in 2014 were 17. Just 17 in the entire world. That’s down 99.9 percent from 3.5 million cases per year in the mid-1980s, and down 80 percent from the same time last year. Some experts believe that the worm could be eradicated as soon as next year.

But is that a good thing? It’s certainly good for humans. But doesn’t each organism play a vital role in a complex ecosystem, even parasites? Might we see an unintended ecological impact if we get rid of the guinea worm?

These are questions that experts like Pieter Johnson, an evolutionary biologist at the University of Colorado in Boulder, have been mulling over for a while. If we were able to eradicate parasites all at once, he says, “It would change ecosystems and food webs in dramatic ways, some of which humans would deem desirable and some less desirable.” Even though they’re often not good guests, parasites play an important role in stabilizing food webs. An animal weakened by a parasite is easier prey for those higher up in the food chain, allowing the predators’ population to grow--so a world without parasites could mean fewer lions, tigers and bears.

However, some species of guinea worms only use humans as hosts. Is the food chain still affected if we get rid of those? Johnson compared the guinea worm’s impending eradication to that of two other infamous plagues: smallpox and rinderpest.

When smallpox was eradicated in 1979, it meant no more victims for a disease that killed an estimated 300 million people in the 20th century. But in recent years pathologists have seen more cases of monkeypox in humans, which usually affects rodents and is related to smallpox. “It’s starting to spread [in humans] because fewer people have that residual resistance,” Johnson says. And, while monkeypox has nowhere near the impact that smallpox had in its prime, Johnson notes that, “it’s doing some interesting things.”

Rinderpest is another disease that humans have successfully eradicated, although it didn’t directly affect us. The virus would infect cattle, buffaloes, deer and other large mammals, killing 95 percent of affected herds. For centuries it has decimated the food supply of any society that relied on cattle as far back as the Roman Empire, and even wiped out 80-90 percent of the cattle in Africa when it was introduced in the late 1800s. It was officially eradicated in 2011. Since rinderpest was not endemic to most of the places it spread to, the impact of its introduction and removal on different ecosystems was dramatic, Johnson says. “We could actually see the dynamics unfold; there were changes in the fire regime, with lion populations, in the grasslands,” Johnson says – the ripples were far-reaching. Such a change wouldn’t be quite so noticeable with the elimination of the guinea worm, he notes, because it’s endemic to the few countries where it still remains.

While the guinea worm may have some small effects on water ecosystems, Johnson is confident that we wouldn’t miss it if it were gone. “My guess is that this is a case where the cost in human suffering is clear,” Johnson says. “The ecological impact is probably small relative to the public health benefit.”

So, no need to lament the guinea worm’s elimination. You can dance on its grave, unworried about future disruptions in the ecosystem. Hopefully its impact will be relegated to terrifying children in sci-fi movies, where it belongs. 

Kepler 22b

Kepler-22b, just 2.4 times the size of Earth, is the first planet known to comfortably circle in the habitable zone of a sun-like star. Scientists do not yet know if the planet has a rocky, gaseous, or liquid composition. It's possible that the world would have clouds in its atmosphere, as depicted here.

NASA/Ames/JPL-Caltech

The world known officially as PSR B1620-26 b orbits a binary star system about 12,000 light-years away. With an estimated age of 12.7 billion years, PSR B1620-26 b is considered one of the oldest planets in the universe, more than twice as old as our solar system. Astronomers found it in the 1990s because of the tug it exerts on its two stars, a pulsar and a white dwarf. 

As a name, PSR B1620-26 b doesn’t exactly have a ring to it, though. Some people instead call it Methuselah, after the oldest living person according to biblical accounts. 

Next year, you’ll be able to vote on that name, and maybe have it officially sanctioned by the International Astronomical Union, in a new project under the Zooniverse. This is a big change for the largest astronomy society in the world, and an exciting one for citizen science. 

To participate, you have to be involved in an astronomy club or non-profit organization, which can register with the IAU and then submit names for about 30 planets of the IAU’s choosing. Voting will happen next spring and summer, and the IAU will announce the new nicknames at a special ceremony at its 29th General Assembly next August, the biggest astronomy meeting on Earth.

In this month’s issue of Popular Science, I argued that the IAU should embrace the public’s desire to get involved like this. The IAU’s Public Naming of Planets and Planetary Satellites Working Group held meetings earlier this summer to that end, and announced the new policy on Wednesday. The IAU approached Chris Lintott, an astronomer and founder of the Galaxy Zoo, precursor to the hugely popular Zooniverse citizen science website. Lintott had already suggested that citizen science could benefit the IAU, according to Lars Lindberg Christensen, the IAU’s press officer. “I’d say it grew organically from our discussions,” Christensen told Popular Science.

Chalk one up for crowdsourcing: With the NameExoWorlds project, we all get to have a say. This is a welcome change, and one that brings us all a little closer to space. But it took a long time and a bit of controversy to get here.

(Possibly) Watery Worlds Of Kepler-62

Two newly discovered planets named Kepler-62e and -f are super-Earths in the habitable zone of a distant sun-like star. The largest planet in the image, Kepler-62f, is farthest from its star and covered by ice. Kepler-62e, in the foreground, is nearer to its star and covered by dense clouds.

David A. Aguilar (CfA)

Since its founding in 1919, the IAU has been the official arbiter of celestial nomenclature. Its members are professional astronomers who choose designations for new moons, asteroids and geologic features on other celestial bodies, so scientists know they’re all talking about the same things. But this power sometimes clashes with public sentiment — most infamously when IAU members essentially demoted Pluto, by changing the definition of planet. 

Tensions flared up again last year, after a new, for-profit astronomy fundraising company called Uwingu (it means “sky” in Swahili) started getting people excited about exoplanets. Astronomers have found thousands of candidate planets in the last five years, with hundreds of them confirmed — but they have pretty boring names, like Kepler-62, HD 40307 g, and our friend PSR B1620-26 b. 

Uwingu sponsored a contest in which people could pay $4.99 to suggest better names, and 99 cents to vote on them. The goal was to build a database of new names while raising money for cash-strapped astronomy research programs.

The IAU took umbrage, reminding Uwingu in a less-than-friendly manner that it was the only organization responsible for such names. Part of the reason for this distaste was the IAU’s long history battling fraudulent companies selling “official” naming rights to stars or lunar real estate. But Uwingu insisted it was different: Profits go to scientific research, it’s run by professional scientists who are IAU members, and it makes no claims of official naming recognition beyond its own purview. Its leaders also pointed out that astronomers and other scientists grant “unofficial” names all the time — there’s a long history of cartoon characters, authors and generally nonsensical names used on the moon and Mars.

The new IAU contest doesn't mention Uwingu by name, but it does include a rule that any participants must be non-profits. By definition, that will exclude Uwingu, which is a for-profit company. There's no reason why a name previously submitted to Uwingu's database can't be submitted in the Zooniverse one, but it would have to come through a non-profit organization.

“The IAU strongly believes that naming of astronomical objects should be free for all and have a wide international participation (which also implies no exchange of funds),” Christensen said.

Let’s Go There!

This is an artist’s interpretation of Kepler-186f, a potentially Earth-like exoplanet.

NASA Ames/SETI Institute/JPL-CalTech

Either way, last year's debate was really larger than a spat between an international organization and American researchers. The more philosophical question was, who owns space? The answer should be all of us. People have been naming planets, stars and landmarks on Earth since time immemorial. Explorers settling the Americas named new cities and mountains for family members, leaders, patrons, hometowns, and themselves, and didn’t get official permission or decree to do so. Why not do the same for the likely billions and billions of exoplanets in the Milky Way? 

Uwingu’s planet contest — and a second one, asking for new names for craters on Mars— involved thousands of people, demonstrating how much the public cares about this. The IAU’s new Zooniverse project is in response to increased public interest, according to the organization. “The intention is that millions of people worldwide will be able to take part in the vote,” the official announcement says. 

There are a couple caveats. In a somewhat surprising twist, the IAU is only using 305 exoplanets that were discovered before Dec. 31, 2008 — so ruling out the 977 planets spotted by the prolific American planet-hunting Kepler Space Telescope, which launched in 2009. By contrast, the COROT space telescope, a French satellite, made several discoveries between first light in January 2007 and the end of 2008.

Christensen said in an email that those older planets are “in general the most reliable exoplanet detections.”

“We are using the first batch of 305 exoplanets to find out how to best work with the public on the naming process. It will take quite some years to name them all, but if all goes well, it is not impossible that the IAU will want to expand with more exoplanet systems,” he said. “Naturally there are no guarantees that all of the 305 exoplanets in this list will stand the test of (more) time. Science changes all the time, and these objects are notoriously hard to detect.”

His point is punctuated by the recent news about Gliese 581 g — what an exciting world it would have been, if it weren’t just a sunspot. 

Once the votes are counted next year, the winning names will be officially sanctioned by the IAU, but they won’t replace the official designations. That just means people will be able to use their nicknames in parallel with the existing nomenclature. So old PSR B1620-26 b will be known as both PSR B1620-26 b and, maybe, Methuselah. 

The Dreaded Speculum:

Causing discomfort in women for hundreds of years.

Matthew Simpson via Flickr CC

By its name alone, the Pap smear sounds like an uncomfortable procedure. Say it aloud: Pap smear. And it’s not too pretty to experience either. You put on a paper dress, slip your feet into stirrups, and spread your legs so a gynecologist can insert a metal duck-bill-shaped speculum (which, if you’re lucky, she’s has taken care to warm up beforehand) into your vagina. Then she swabs your cervix with a long Q-tip to collect a few cells, which she’ll examine under the microscope for abnormal growth that could develop into cancer.

It’s a procedure inconvenient and uncomfortable enough that many women chronically avoid having it done, despite the recommendation to get the cervical cancer test every three years. But it’s incredibly important for women’s health: since the Pap smear’s introduction in the 1950s, cervical cancer diagnoses and deaths have gone down 60 percent, saving thousands upon thousands of lives.

But the classic test now has some competition. In late April, the FDA approved a new test to be used interchangeably with (or replace) the Pap smear to screen for cervical cancer. Where the Pap looks for early signs of cancer in cervical cells, the new test, called the “cobas HPV test,” looks for a common cause of cervical cancer: human papillomavirus (HPV). HPV is a very common sexually transmitted disease, carried by 40 percent of U.S. women ages 14 to 59 at any given time, that causes around 90 percent of all cervical cancers.

Pap Smear.

The clump on the left are normal cervical cells. The ones on the right are infected with human papillomavirus, a frequent cause of cervical cancer.

Ed Uthman via Flickr CC

However, the trial may have overlooked a particularly high-risk group: young women between the ages of 25 and 29. So says a coalition of 17 patient and women’s health groups, which sent a letter to the FDA opposing the test’s approval. As a group, women ages 25 to 29 are more likely to carry HPV but less likely to have cancer, putting them at high risk for receiving a false positive on the new test. These women are then sent in for unnecessary follow-up procedures that could do them physical harm and scare them away from returning to the gynecologist for their next check-up.

This extra risk to younger women should be evident from the clinical trial data. But because it included relatively few women ages 25 to 29 and only observed them for three years, the test’s ineffectiveness in this age group is hidden, the coalition says.

“The risks that come with this decision really affect younger women more than others,” said Anna Mazzucco, scientific advisor at the National Center for Health Research, who organized the coalition’s letter. “That's why we're so concerned that there were not enough data on young women. We really do not understand this decision.”

There are more than 100 known strains of HPV, and around 40 of them are transmitted sexually. Most show no symptoms and are incredibly common, especially in women, but a handful of them can cause cervical cancer. When these strains of HPV infect cervical cells, they can cause those cells to grow abnormally and, over 10 to 15 years, those abnormal cells can develop into cancer.

Most HPV viruses, however, clear up on their own within two years. By the time a woman reaches her thirties, most of the strains collected in her sexually active twenties should have resolved themselves. The viruses that stick around for more than a few years are the ones to worry about; those are the ones that have managed to escape her immune system and continue to drive abnormal cell growth.

A Pap smear can detect those abnormally growing cells at a very early stage, when they are growing strangely but are not yet cancerous. That is why both cancer deaths and diagnoses went down after its introduction.

The cobas HPV test, on the other hand, detects the 14 strains of HPV that present the highest cancer risk, including two strains (HPV-16 and HPV-18) that alone cause around 70 percent of cervical cancers. Like the Pap smear, it relies on a swab of cells from a woman’s cervix. But instead of identifying precancerous cells, it detects the DNA of these cancer-causing viruses.

Roche compared its test with the standard in its clinical trial by taking cervical swabs from some 40,000 women, and sending each sample for both a Pap smear and cobas HPV test. Around 10.5 percent of the women in the study, ranging from age 25 to greater than 50 years, were positive for HPV, while 6.4 percent had an abnormal Pap smear. Women who tested positive with either method received additional screening to confirm whether they really had precancerous cells or if it was a false positive. When the results from all ages were pooled, the cobas HPV test was able to identify more women with early signs of cancer, according to Roche’s data.

The data Roche presented to the FDA did not break down the results by age, but there is reason to be concerned that young women were not well represented. Despite their increased risk, only 16 percent of the women were ages 25 to 29; compare that to the 54 percent of women older than 40 years. And those younger women tested positive for HPV almost twice as frequently: 21.1 percent versus 11.6 percent of women 30-39 years old.

In which case, we’d want to know how many of those young women actually went on to develop cancer, and how many of the HPV cases cleared up on their own. But the trial only lasted for three years, which is not long enough to know. Most cervical cancer takes 10 to 15 years to develop, so Roche never detected full-fledged cancers, just different stages of precancerous growth which might never lead to cancer.

There’s an argument that sending some women for extra treatment who don’t need it is a small price to pay if it means catching more cases of cancer overall. But this disregards the harms of excess screening and unnecessary care, the coalition argues.

One risk of the further screening for cervical cancer is fertility damage. While the second tier of cervical cancer testing after a Pap smear or HPV test is harmless, the next stage—a tissue biopsy—can weaken the cervix. A weaker cervix can lead to trouble in future pregnancies, such as causing early labor or, in the worst case, a miscarriage. “If you start sending more women for [follow-up screening], that stacks the odds for more aggressive treatment than she actually needs,” said Mazzucco. This affects younger, pre-menopausal women more than others, since they still have a future of childbearing ahead of them.

The second and perhaps more pertinent risk is anxiety. After a woman gets an abnormal Pap result, the following period of not knowing if she has cancer can be very stressful. A 2003 survey found that 59 percent of women experienced anxiety after an abnormal Pap, with that anxiety affecting daily life for 30 percent. If the mere presence of HPV is enough to signal cancer, these anxious periods will be more frequent—possibly making women dread going to their annual checkups at all.

“There's a lot of research that says: the major population of women who actually get cervical cancer are women who have never had a Pap smear or haven't had one in the last five years,” Mazzucco said. “We feel that [using the cobas HPV test as a primary test for cervical cancer] could reduce the number of women who get screened, which is not going to prevent more cases of cervical cancer.”

Additionally, the trial did not include many women who had been vaccinated for HPV—a growing cohort in the U.S. as teens who were vaccinated reach adulthood. (The vaccine had been administered to 56 million young women in the U.S. as of 2012.)

Will a test for HPV still be a good test for cervical cancer as more women are vaccinated for high-risk strains? We don’t know because less than two percent of women in the trial were vaccinated.

Another concern is that, while HPV causes most cervical cancers, it doesn’t cause them all. According to a 2014 survey, some 9.4 percent of cervical cancers are unrelated to HPV, while 3.2 percent are caused by rare types of HPV that aren’t detected by the test. If the cobas HPV test is used alone, those cases of cancer would fly under the radar.

That’s why, ideally, the cobas HPV test and the Pap smear would be paired together in women older than 30, says Mazzucco. They can be used on the same cervical swab, and the FDA has already approved them to be used together. A positive HPV test with a negative Pap would delay additional invasive procedures, while a positive Pap with a negative HPV test would call for further follow-up. But the HPV test should never be used as a diagnostic tool for cancer in women younger than 30 years, she says.

Luckily for the concerned parties, the FDA doesn’t tell doctors what to do. Instead, major medical societies, such as the American Congress of Obstetricians and Gynecologists, will use the approval information to develop guidelines for how these tests should be used in practice. Despite the FDA approval, they could decide to not promote use of the cobas HPV test alone to test for cervical cancer. “Primary HPV testing does not replace the Pap test, and it is extremely unlikely that doctors will stop using the Pap any time soon,” wrote the Society of Gynecologic Oncology in a statement after the cobas HPV test approval.

So what does this mean for you? When you’re going to the gynecologist, ask questions. If your doctor takes a cervical swab, find out what kind of testing she’s doing—a Pap smear, HPV test, or both. Walk through the different scenarios, informed by your own sexual behavior, to help you prepare for what a positive result on the tests would mean and the next steps you’d take. If you’re sexually active and have a positive HPV test, ask for a Pap smear as well so you have as much information as you can get.

The most important thing is to just keep going in for testing. Start in your twenties so that you get used to the process and it feels less stressful. It can be easy to panic if you get a positive result, but keep in mind that it takes a decade for that HPV strain or abnormal Pap result to develop into cancer. If you get tested regularly and find it early, you have already done the best you can for yourself.

LadyBits is a collective of tech-savvy writers, editors, and innovators breaking through barriers in the journalism industry.

Dinitrophenol in the 1930s

U.S. Food and Drug Administration

In 2012, Sean Cleathero died from drinking an explosive/pesticide mixed with water. His gym had sold it to him as a weight loss drug. The mixture gave him a fever of over 107 degrees and killed him within eight hours, even after he received care at the Wycombe Hospital outside of London.

The case came up in the news again recently because three men who worked at the gym are on trial for manslaughter. A few weeks ago, a review of data from the U.K.'s National Poisons Information Service linked 30 complaints and five deaths to the same substance Cleathero drank. What were all these adults doing chugging an industrial chemical? They were following the advice of 1) some Stanford University doctors from the 1930s and/or 2) forums on the Internet.

Scientifically known as 2,4-dinitrophenol, the chemical actually does make people lose weight. Only it does so in a terrifying way. It decouples the two reactions that the cells' powerhouse, its mitochondria, use to turn food into energy. Starved for resources, the cells in the body start consuming fat in the body. So far, so good, right? But what happens to all that energy the mitochondria would have made?

Instead of turning it into useable energy molecules, called ATP, it's transformed into excess heat. Those who take dangerous doses of dinitrophenol raise their internal body temperatures to such an extent that it damages the protein in their bodies. Think of how an egg white changes when you heat it by boiling it or frying it. Egg whites are nearly all protein; how they react to heat is how your body's proteins react to heat. Very high doses of dinitrophenol can cause immediate rigor mortis after death.

DNP (as it's also known) has some other effects, too, including liver and kidney problems and cataracts. Doctors have known about these effects for decades. Remember those 1930s Stanford doctors? They were the first to try to treat their obese patients with dinitrophenol. They didn't make the chemical; they knew about it from dye and munitions factories, which used it. One of the problems munitions factory workers suffered was weight loss, they knew. And they knew workers sometimes died, too. It seems they thought they could avoid deaths by closely supervising their patients, but they underestimated how word would spread and people would want to treat themselves.

After the Stanford team published its first papers on treating obesity with dinitrophenol, a small craze for the chemical followed. People bought it over the counter at drugstores. Enough of them suffered ill effects that the U.S. Food and Drug Administration declared dinitrophenol illegal to sell for human consumption in 1938. The idea of using DNP for weight loss disappeared for a while.

It popped up again at least once before now, when a doctor re-discovered the Stanford papers in the 1980s and opened a clinic in Texas. The FDA shut him down.

It's unclear who "discovered" the papers yet again more recently, but it is clear the Internet had a role. The papers are easy to find online and wonderful to read. They have little jargon. They so naively refer to World War I as "the war." They state dosages. But how do you know how much you're actually getting in that pill you order off the Internet? Or what dose is right for you? Tolerances vary widely.

The earliest, post-1980s report I found of someone dying after consuming DNP to lose weight was published in 2004. Several reports followed, but so did things like YouTube videos of before and after pictures of dinitrophenol users and detailed guides on bodybuilder forums. Bodybuilders' websites sold the chemical in pill form.

Perhaps DNP will disappear again soon, however. A number of U.K. newspapers have reported on DNP-related deaths. I saw a lot of YouTube comments on DNP videos trying to warn others away. So while the Internet made it possible for the idea to spread more widely than it ever did in the 1930s or 1980s, maybe our connectivity will also help spread word of DNP's dangers. 

A (large) kidney stone, measuring about 0.3 inches in diameter.

Robert R. Wal via Wikimedia Commons

The hotter weather expected with climate change is likely to cause a litany of figurative aches for humanity (and already is), but some of those pains may be quite literal. A new study found that higher temperatures significantly increase the risk of developing kidney stones, hard crystals that are painful to pass and which can cause damage to the organs. The idea is that hotter weather leads people to become more dehydrated, which allows minerals to concentrate and crystalize within the body.

"We found that as daily temperatures rise, there is a rapid increase in the probability of patients presenting over the next 20 days with kidney stones," said study lead author Dr. Gregory Tasian, a pediatric urologist and epidemiologist at The Children's Hospital of Philadelphia, in a statement.

The study, published in the journal Environmental Health Perspectives, examined the health records of more than 60,000 people in several American cities, along with weather records. People were most likely to show up at the hospital with kidney stones three days after high temperatures. In Chicago, Atlanta, and Dallas (the winner of the dubious prize for most stones), people were nearly 40 percent more likely to seek medical help for the condition at temperatures of 86 degrees Fahrenheit compared to when it was only 50°F  outside.

Kidney stones have become more common in the recent past, as temperatures have risen, a trend that is likely to continue, the scientists wrote.  About one in 11 people have had kidney stones, whereas they were only found in about one in 20 people in 1994. Interestingly, the really hot days seem to make a difference, as opposed to the average conditions, as CBS News noted: 

Kidney stones usually do not cause permanent damage, and can be dealt with by drinking a lot of water and taking pain medication. But they sometimes do require surgery to treat, and tend to recur in a significant percentage of people who get them.

Signs like this were used to show which houses had received the smallpox vaccine

PAHO

Earlier this week, the U.S. Centers for Disease Control and Prevention announced something surprising: Federal researchers discovered six 60-year-old vials with smallpox virus in them. The vials were in a forgotten freezer in a lab on the Bethesda, Maryland, campus of the U.S. National Institutes of Health. According to international agreement, samples of smallpox are only supposed to be kept in two high-security facilities in the world, one at the CDC in Atlanta and one in Russia. Whoops.

You can learn more about the find in Popular Science's report from Tuesday. Today, we talked with experts to answer some of our deeper questions about those six vials. For example, we learned why the CDC plans to grow and study the virus before destroying it, and whether discoveries like this have happened before. (They have.)

Why is smallpox such a big deal?

Although now eradicated, smallpox was one of the deadliest illnesses to infect humans. It passed easily between people. Depending on what strain they got, 30  to nearly 100 percent of people who caught the virus died. And the world is now more vulnerable to smallpox than ever. Countries have stopped routinely immunizing children against the disease. Meanwhile, the effect of the smallpox vaccine wears off over time, so older folks who received the vaccine as kids aren't fully protected anymore.

Some experts think it's possible that terrorists may try to steal samples of unsecured smallpox to make a biological weapon… or that an unwitting researcher may open a forgotten vial and release its contents, sickening herself and others around her. "None of these [scenarios] are likely," says Erik Heegaard, who runs his own biosecurity consulting firm in Denmark. "But it's possible."

Should I be worried?

No, it doesn't appear that any researchers or members of the public are at risk of getting sick from these vials. It also doesn't appear that anybody has taken or used the vials since they were prepared in the 1950s. At that time, smallpox was a common illness circulating among people, so it wasn't unusual for a lab to keep some in its freezers.

In addition, Heegaard thinks the FDA, NIH and CDC handled the discovery safely. "This is the best setting you could hope for because it's the most controlled environment ever," he says.

Has this happened before? Is it likely to happen again?

Scientists have discovered forgotten smallpox samples before, but the when and where of the incidents are difficult to confirm. All the experts I talked with said they had heard of cases, but weren't sure if this or that rumor were true, or didn't have documentation handy. A spokesperson at the Sandia National Laboratories, which study biosecurity, pointed to two cases that Nature magazine covered. One occurred in the 1990s, in an Eastern European lab. The other occurred after that, at the Swiss Serum and Vaccine Institute in Bern.

Experts believe it's likely there are still many freezers around the world holding forgotten smallpox. "This is a scenario that was foreseen," says Jennifer Guadioso, the head of the International Biological Threat Reduction Program at Sandia. "It was not a big surprise. Obviously, we didn't predict that FDA or NIH would be the laboratory."

Even with these cases, however, nobody has gotten sick from smallpox since 1978. Samples that are properly sealed won't infect people and it's easy to destroy found samples by incinerating them.

Surprise discoveries also occur with other pathogens that are normally kept under high security. In 2009, the U.S. Army Medical Research Institute of Infectious Diseases temporarily suspended its research into dangerous pathogens because officials feared their records didn't match what they actually had. "I believe that the probability that there are additional vials of BSAT [biological select agents and toxins] not captured in our AIMS database is high," Colonel John Skvorak, then the institute's director, told the Frederick News-Post. BSAT could include organisms such as plague and anthrax.

As time passes, the risk that these forgotten samples will infect anybody decreases. Forgotten freezers may suffer from electricity blackouts or maintenance issues, which would warm and kill their contents. In addition, the smallpox virus, although robust, must eventually become unable to reproduce. In fact, CDC tests on these newfound vials may help scientists learn more about just how long frozen smallpox virus is able to stay infectious.

How do you just forget you have a sample of smallpox?

In the 1950s and 1960s, even labs handling dangerous biological materials didn't have as strict of inventory procedures as they do today. In an older lab, a past scientist could have easily stashed pathogens without leaving any record of doing so.

It's normal for scientists to store many samples, too. Your own author left behind racks of gross, but not dangerous, genetic samples when she left UCLA's Flylab. (Sorry, Dr. Olson!) As many scientists told me, the attitude is, What if I or someone else needs this again someday?

What's going to happen to the vials now?

The CDC will try to grow the contents of the vials in petri dishes, to see if they're still able to reproduce after sitting around for 60 years. This is a question of scientific interest. It also helps security experts determine how worried they should be about other forgotten samples around the world.

CDC scientists will also perform experiments to try to determine where the found samples came from and how they ended up in Bethesda. Heegaard believes the centers will want to read the entire DNA sequence of the virus. CDC spokesperson Benjamin Haynes wasn't sure if DNA sequencing was in the works. "I know they are going to be tested and characterized," he says.

Then the vials will be destroyed. They'll go into an autoclave, a machine scientists routinely use to sterilize their equipment, and be incinerated.