By combining genes from different bacteria species, scientists created E. coli that can produce diesel fuel from fat. Image via Marian Littlejohn/PNAS

Over the past few decades, researchers have developed biofuels derived from an remarkable variety of organisms—soybeans, corn, algae, rice and even fungi. Whether synthesized into ethanol or biodiesel, though, all of these fuels suffer from the same limitation: They have to be refined and blended with heavy amounts of conventional, petroleum-based fuels to run in existing engines.

Though this is far from the only current problem with biofuels, a new approach by researchers from the University of Exeter in the UK appears to solve at least this particular issue with one fell swoop. As they write today in an article in Proceedings of the National Academy of Sciences, the team has genetically engineered E. coli bacteria to produce molecules that are interchangeable to the ones in diesel fuels already sold commercially. The products of this bacteria, if generated on a large-scale, could theoretically go directly into the millions of car and truck engines currently running on diesel worldwide—without the need to be blended with petroleum-based diesel.

The group, led by John Love, accomplished the feat by mixing and matching genes from several different bacteria species and inserting them into the E. coli used in the experiment. These genes each code for particular enzymes, so when the genes are inserted into the E. coli, the bacteria gains the ability to synthesize these enzymes. As a result, it also gains the ability to perform the same metabolic reactions that those enzymes perform in each of the donor bacteria species.

By carefully selecting and combining metabolic reactions, the researchers built an artificial chemical pathway piece-by-piece. Through this pathway, the genetically modified E. coli growing and reproducing in a petri dish filled with a high-fat broth were able to absorb fat molecules, convert them into hydrocarbons and excrete them as a waste product.

Hydrocarbons are the basis for all petroleum-based fuels, and the particular molecules they engineered the E. coli to produce are the same ones present in commercial diesel fuels. So far, they’ve only produced tiny quantities of this bacterial biodiesel, but if they were able to grow these bacteria on a massive scale and extract their hydrocarbon products, they’d have a ready-made diesel fuel. Of course, it remains to be seen whether fuel produced in this way will be able to compete in terms of cost with conventional diesel.

Additionally, energy never comes from thin air—and the energy contained within this bacterial fuel mostly originates in the broth of fatty acids that the bacteria are grown on. As a result, depending on the source of these fatty acids, this new fuel could be subject to some of the same criticisms leveled at biofuels currently in production.

For one, there’s the argument that converting food (whether corn, soybeans or other crops) into fuel causes ripple effects in global food market, increasing the volatility of food prices, as a UN study from last year found. Additionally, if the goal of developing new fuels is to fight climate change, many biofuels fall dramatically short, despite their environmentally-friendly image. Using ethanol made from corn (the most widely used biofuel in the U.S.), for example, is likely no better than burning conventional gasoline in terms of carbon emissions, and maybe actually be worse, due to all the energy that goes into growing the crop and processing it info fuel.

Whether this new bacteria-derived diesel suffers from these same problems largely depends upon what sort of fatty acid source is eventually used to grow the bacteria on a commercial scale—whether it would by synthesized from a potential food crop (say, corn or soy oil), or whether it could come from a presently-overlooked energy source. But the new approach already has one major advantage: Just the steps needed to refine other biofuels so they can be used in engines use energy and generate carbon emissions. By skipping these steps, the new bacterial biodiesel could be an energy efficient fuel choice from the start.

A mixture of plant oils, bacterial spores and ozone is responsible for the powerful scent of fresh rain. Image via Wikimedia Commons/Juni

Step outside after the first storm after a dry spell and it invariably hits you: the sweet, fresh, powerfully evocative smell of fresh rain.

If you’ve ever noticed this mysterious scent and wondered what’s responsible for it, you’re not alone.

Back in 1964, a pair of Australian scientists (Isabel Joy Bear and R. G. Thomas) began the scientific study of rain’s aroma in earnest with an article in Nature titled “Nature of Agrillaceous Odor.” In it, they coined the term petrichor to help explain the phenomenon, combining a pair of Greek roots: petra (stone) and ichor (the blood of gods in ancient myth).

In that study and subsequent research, they determined that one of the main causes of this distinctive smell is a blend of oils secreted by some plants during arid periods. When a rainstorm comes after a drought, compounds from the oils—which accumulate over time in dry rocks and soil—are mixed and released into the air. The duo also observed that the oils inhibit seed germination, and speculated that plants produce them to limit competition for scarce water supplies during dry times.

These airborne oils combine with other compounds to produce the smell. In moist, forested areas in particular, a common substance is geosmin, a chemical produced by a soil-dwelling bacteria known as actinomycetes. The bacteria secrete the compound when they produce spores, then the force of rain landing on the ground sends these spores up into the air, and the moist air conveys the chemical into our noses.

“It’s a very pleasant aroma, sort of a musky smell,” soil specialist Bill Ypsilantis told NPR during an interview on the topic. “You’ll also smell that when you are in your garden and you’re turning over your soil.”

Because these bacteria thrive in wet conditions and produce spores during dry spells, the smell of geosmin is often most pronounced when it rains for the first time in a while, because the largest supply of spores has collected in the soil. Studies have revealed that the human nose is extremely sensitive to geosmin in particular—some people can detect it at concentrations as low as 5 parts per trillion. (Coincidentally, it’s also responsible for the distinctively earthy taste in beets.)

Ozone—O_3, the molecule made up of three oxygen atoms bonded together—also plays a role in the smell, especially after thunderstorms. A lightning bolt’s electrical charge can split oxygen and nitrogen molecules in the atmosphere, and they often recombine into nitric oxide (NO), which then interacts with other chemicals in the atmosphere to produce ozone. Sometimes, you can even smell ozone in the air (it has a sharp scent reminiscent of chlorine) before a storm arrives because it can be carried over long distances from high altitudes.

But apart from the specific chemicals responsible, there’s also the deeper question of why we find the smell of rain pleasant in the first place. Some scientists have speculated that it’s a product of evolution.

Anthropologist Diana Young of the University of Queensland in Australia, for example, who studied the culture of Western Australia’s Pitjantjatjara people, has observed that they associate the smell of rain with the color green, hinting at the deep-seated link between a season’s first rain and the expectation of growth and associated game animals, both crucial for their diet. She calls this “cultural synesthesia”—the blending of different sensory experiences on a society-wide scale due to evolutionary history.

It’s not a major leap to imagine how other cultures might similarly have positive associations of rain embedded in their collective consciousness—humans around the world, after all, require either plants or animals to eat, and both are more plentiful in rainy times than during drought. If this hypothesis is correct, then the next time you relish the scent of fresh rain, think of it as a cultural imprint, derived from your ancestors.

Ribbon worms come in all shapes and sizes. This one, with white stripes along the body, was found off the coast of Mexico. Photo by Chris Meyer and Allen Collins

Whether they’re on a rain-soaked sidewalk, in the compost bin or on the end of a fish hook,  the worms most people know are of the segmented variety. But what about all the other worms out there?

With more than 1,000 species of ribbon worms (phylum Nemertea), most found in the ocean, there is a huge range of sizes and lifestyles among the various types. A defining characteristic of ribbon worms is the presence of a proboscis—a unique muscular structure inside the worm’s body. When attacking prey, they compress their bodies to push out the proboscis like the finger of a latex glove turned inside-out.

Here are 14 other fun facts about them:

1. The largest species of ribbon worm is the bootlace worm, Lineus longissimus, which can be found writhing among rocks in the waters of the North Sea. Not only is it the largest nemertean, but it may also be the longest animal on the planet! Uncertainty remains because these stretchy worms are difficult to accurately measure, but they have been found at lengths of over 30 meters (98 feet) and are believed to even grow as long as 60 meters (197 feet)—longer than the blue whale! Despite their length they are less than an inch around.

An illustration of a bootlace worm, which can be found at lengths of 30 meters (98 feet) or longer. From McIntosh/Publisher Selam Amare

2. The smallest ribbon worm species is less than a centimeter long, and resembles a piece of thread more closely than what we think of as a worm.

3. Ribbon worms have highly developed muscles that allow them to contract their bodies, shrinking to a tenth of their extended length when threatened.

4. Talk about stretching: ribbon worm muscles don’t just contract–they can also expand, allowing some species to swallow prey (such as other kinds of worms, fish, crustaceans, snails and clams) that are more than double the width of their narrow bodies

Ribbon worm (Nemertean) eating a polychaete annelid [edited] from LabNemertea on Vimeo.

5. The proboscis varies among the species. Some are sticky or have suckers to help grasp prey, and some species, like those in the order Hoplonemertea, even stab their prey with a sharp spike, called a stylet, on the proboscis.

6. Because the stylets often are lost during an attack, the worms continually make and use replacements that they have in reserve in internal pouches.

7. As a second line of defense, many ribbon worms are poisonous and taste bad. Several species contain tetrodotoxin, the infamous pufferfish venom that can induce paralysis and death by asphyxia. It’s still not known exactly how the toxins are produced—they may linger in the worms from ingested bacteria—but they deter predators from taking a bite. Some even eject toxins from their proboscis.

8. Some ribbon worms sneak up on their prey, lying in wait buried in the sandy seafloor. One species of worm will pop up from its home in the sand when a fiddler crab walks over. The worm will cover the prey with toxic slime from its proboscis, paralyzing the crab so the ribbon worm can slide into a crack in the shell and eat the crab from the inside out.

9. Not all ribbon worms are predators – some are parasites. One genus of ribbon worms, Carcinonemertes, lives as a parasite on crabs, eating the crab’s eggs and any animals that it can find from the confines of its host.

A parasitic ribbon worm, seen in this picture with the crab eggs it persists on.
Photo by Sadeghian and Santos

10. Most ribbon worms produce a slippery mucus that covers their bodies and helps them to navigate through the mud and rocks on the ocean floor.

11. Some also use the mucus as a protective coat to keep from drying out when exposed to air during low tides. Others use their proboscis to move by attaching it to an object and pulling themselves forward. This same mucus makes them hard to catch! And not only by predators: scientists trying to catch the worms have a difficult time.

12. Marine ribbon worms usually have separate sexes and temporary sex organs. Rows of gonads line the inside of their bodies to produce either eggs or sperm. When they are ready to be released, the gonad ducts form on demand and are reabsorbed after reproduction.

13. Most ribbon worms have direct development: a miniature version of the worm hatches from a fertilized egg. However, the young of one group of ribbon worms, the heteronemerteans, emerge in a bizarre larval stage that looks like a flying saucer. After a few weeks to months living and feeding in the open ocean, a small worm develops inside and, when it’s ready, it eats its way out of the original larva encasing. Then the worm falls to the sea floor where it spends the rest of its life.

14. Many ribbon worms can regenerate when a predator takes a bite, healing their broken ends. One worm species, Ramphogordius sanguineus, has an exceptional ability to regenerate: if any part of their body is severed (except for the very tip of their tail where there are no nerves), it can regrow into a new worm. This new individual may be smaller than the worm it came from, but more than 200,000 worms can result from an individual that is only 15 centimeters (6 inches) long!

 Learn more about the ocean from the Smithsonian’s Ocean Portal. 

One of the Cornell team’s prosthetic ears, created from living cartilage cells. Image via PLOS ONE/Reiffel et. al.

3D printing is big news: During his State of the Union speech, President Obama called for the launch of manufacturing hubs centered around 3D printing, while earlier this week, we saw the birth of one of the most playful applications of the technology yet, the 3D Doodler, which lets you draw solid plastic objects in 3 dimensions.

Yesterday, Cornell doctors and engineers presented a rather different use of the technology: a lifelike artificial ear made of living cells, built using 3D printing technology. Their product, described in a paper published in PLOS ONE, is designed to help children born with congenital defects that leave them with underdeveloped outer ears, such as microtia.

The prosthesis—which could replace previously used artificial materials with styrofoam-like textures, or the use of cartilage tissue harvested from a patient’s ribcage—is the result of a multistep process.

First, the researchers make a digital 3D representation of a patient’s ear. For their prototype, they scanned healthy pediatric ears, but theoretically, they might someday be able to scan an intact ear on the other side of a patient’s head—if their microtia has only affected one of their ears—and reverse the digital image, enabling them to create an exact replica of the healthy ear.

Next, they use a 3D printer to produce a solid plastic mold the exact shape of the ear and fill it with a high-density collagen gel, which they describe as having a consistency similar to Jell-O.

A 3D printer creates a plastic mold for the ear’s collagen scaffolding. Image via Lindsay France/Cornell University Photography

A collagen ear, to be seeded with living cartilage cells and implanted under skin. Image via Lindsay France/Cornell University Photography

After printing, the researchers introduce cartilage cells into the collagen matrix. For the prototype, they used cartilage samples harvested from cows, but they could presumably use cells from cartilage elsewhere on the patient’s own body in practice.

Over the course of a few days in a petri dish filled with nutrients, the cartilage cells reproduce and begin to replace the collagen. Afterward, the ear can be surgically attached to a human and covered with skin, where the the cartilage cells continue to replace the collagen.

So far, the team has only implanted the artificial ears underneath the skin on the backs of lab rats. After 3 months attached to the rats, the cartilage cells had replaced all the collagen and filled in the entire ear, and the prosthetic retained its original shape and size.

In a press statement, co-author Jason Spector said that using a patient’s own cells would greatly reduce the chance of the body rejecting the implant after surgery. Lawrence Bonassar, another co-author, noted that in addition to congenital defects, the prosthesis could also be valuable for those who lose their outer ear as a result of cancer or an accident. If used for a child with microtia, the ear won’t grow along with the head over time, so the researchers recommend waiting to implant one of their prostheses until the patient is 5 or 6 years old, when ears have normally grown to more than 80 percent of their adult size.

The biggest advantage of the new technology over existing methods is the fact that the production process is customizable, so it could someday produce remarkably realistic-looking ears for each patient on a rapid timescale. The researchers have actually sped up the process since conducting the experiments included in the study, developing the ability to directly print the ear using the collagen as an “ink” and skip making the mold.

There are still a few problems to tackle, though. Right now, they don’t have the means to harvest and cultivate enough of a pediatric patient’s own cartilage to build an ear, which is why they used samples from cows. Additionally, future tests are needed to prove that surgical implantation is safe for humans. The team says they plan to address these issues and could be working on the first implant of such an ear in a human as soon as 2016.

A new study indicates that mosquitoes can become habituated to the smell of DEET over time, reducing its effectiveness as a repellent. Image via CDC

If you’re someone that’s naturally irresistible to mosquitoes, a new finding published today in PLOS ONE could make for a rude awakening. A group of researchers from the London School of Hygiene and Tropical Medicine discovered that three hours after an exposure to DEET, many Aedes aegypti mosquitoes were immune to the chemical, ignoring its typically noxious smell and attempting to land on irresistible human skin.

Normally, DEET—short for N,N-Diethyl-meta-toluamide, which is the active ingredient in most insect repellents on the market—works because mosquitoes seem to find the chemical’s smell unpleasant and actively avoid landing on surfaces where it has been applied. But in this study, led by Nina Stanczyk, the researchers found mosquito behavior that runs contrary to scientists’ previous understanding of how the insects interact with the chemical.

DEET is used in the majority of insect repellents on the market. Image via Flickr user Spokenhope

Initially, the researchers split a number of Aedes aegypti mosquitoes (a common species found on all continents, including North America) into two groups, each in a metal mesh cage. Then they had volunteers hold their arms about an inch over each cage, with one treated with a 20-percent DEET solution and another that had no repellent (a control arm).

Three hours later, they repeated the experiment, and counted exactly how many mosquitoes overcame the DEET and attempted to get through the metal mesh to reach the arms. They found that about half of the mosquitoes who’d been initially exposed to DEET on their first go-round seemed immune to the chemical during the second trial and tried to reach the DEET-covered arm, compared to the 10-20 percent that had attempted to do so during their first trial. This number was still less than the proportion of mosquitoes trying to reach the plain arm (70-80 percent).

Further proof the development of DEET immunity, though, lies in a third group of mosquitoes, who were exposed to a control arm first and a DEET arm second. Because they hadn’t had the chance to become habituated to the chemical, a much lower amount of them (less than 10 percent) tried to reach the DEET-covered arm.

To ensure that some sort of interaction between chemicals in human skin and DEET wasn’t responsible, the researchers also replicated the experiment with a heating device—to which mosquitoes are naturally attracted—that was also covered in DEET. The results were similar, indicating that the insects were somehow becoming habituated to DEET itself, regardless of the surface it was covering.

So why did the mosquitoes, as a whole, overcome their dislike of DEET? Previous studies by this group and others have found particular mosquitoes with a genetic mutation that made them innately immune to DEET, but they say that this case is different, because they didn’t demonstrate this ability from the start.

They suspect, instead, that the insects’ antennae became less chemically sensitive to DEET over time, as evidenced by electroantennography on the mosquitoes’ odor receptors after each of the tests—a phenomenon not unlike a person getting used to the smell of, say, the ocean or a manufacturing plant near his or her house.

Of course, this sort of aromatic habituation is significantly less convenient, because DEET-based repellents are relied upon not just to help us avoid irritating bites but also to stop the spread of mosquito-borne diseases like malaria and dengue. But the researchers don’t recommend dropping DEET entirely, for a few reasons.

For one, mosquitoes live as adults for only a few days at most, and the habituation likely isn’t passed along to offspring, so the odds that a particular mosquito you come across has already been exposed to DEET is pretty low. Additionally, even if it has, not all of the individual mosquitoes in the trial became used to the DEET, so it should still be somewhat effective as a repellent.

Most important, though, is the fact that we still haven’t developed any other repellent that is as consistently potent as DEET—so for now, they say, people living in areas with high risks of mosquito-borne illnesses have little other choice than to keep using it.

A study shows that wild perch are less fearful, eat faster and are more anti-social when exposed to a common pharmaceutical pollutant. Image via Bent Christensen

It’s obvious that anti-anxiety medicines and other types of mood-modifying drugs alter the behavior of humans—it’s what they’re designed to do. But their effects, it turns out, aren’t limited to our species.

Over the past decade, researchers have repeatedly discovered high levels of many drug molecules in lakes and streams near wastewater treatment plants, and found evidence that rainbow trout and other fish subjected to these levels could absorb dangerous amounts of the medications over time. Now, a study published today in Science finds a link between behavior-modifying drugs and the actual behavior of fish for the first time. A group of researchers from Umeå University in Sweden found that levels of the anti-anxiety drug oxazepam commonly found in Swedish streams cause wild perch to act differently, becoming more anti-social, eating faster and showing less fear of unknown parts of their environment.

The research group, led by ecologist Tomas Brodin, put wild perch in water with 1.8 micrograms of oxazepam diluted per liter—a level consistent with samples taken from surface waters near human development around Sweden. After 7 days swimming in the contaminated water, the perch had levels of the drug in their tissues that were similar to those of wild perch samples, indicating that the pharmaceutical was being absorbed into their bodies at rates similar to what’s happening in rivers and streams.

When they closely observed the behavior of these contaminated fish, the results were unmistakable. Those dosed with the anti-anxiety drug were more active, more willing to explore novel parts of their environment and more likely to swim away from the rest of their group as compared to fish that were kept in pristine waters. They also ate faster, finishing a set amount of plankton in a shorter time.

The researchers also included a third group of fish, exposed to levels of the drug way higher than those present in the environment. All of the changes shown in the fish exposed to the mild level of the drug were greatly exaggerated in this group, indicating that the drug was indeed responsible for the behavioral changes observed.

The idea of drug-addled fish might be funny, but the researchers say it could be a troubling sign of the way mounting levels of water-borne pharmaceuticals are affecting natural ecosystems. Because perch and other predator fish play a key role in food webs, altered foraging behavior—say, eating more prey—could lead to proliferation of the algae that their prey typically eat, upsetting an ecosystem’s balance as a whole. Or, if wild perch are engaging in more risky behavior (exploring parts of their environment they usually shy away from) it could lower the species’ survival rate.

Additionally, the research group worries that the drug could affect a broad spectrum of wildlife, because the particular receptor it binds to in the brain is widely distributed among aquatic species. And Oxazepam is far from the only drug that’s been found to pollute aquatic ecosystems—in the U.S., traces of over-the-counter painkillers, birth control hormones and illegal drugs have all been detected. “That environmentally relevant concentrations of a single benzodiazepine [oxazepam] affect fish behavior and feeding rate is alarming, considering the cocktail of different pharmaceutical products that are found in waters worldwide,” the researchers note in the paper.

These drug molecules can enter the environment in a few different ways. The practice of flushing old pills down the toilet is the first that probably comes to mind—and the easiest to prevent—but many pharmaceutical pollutants result from drug molecules that are ingested properly, go through the human body, pass out in urine and make it through wastewater treatment plants and into the environment. ”The solution to this problem isn’t to stop medicating people who are ill but to try to develop sewage treatment plants that can capture environmentally hazardous drugs,” Jerker Fick, one of the paper’s co-authors, said in a statement.

Chromodoris reticulata, native to the Pacific, engages in mating behavior unknown in the rest of the animal kingdom. Image via Stephen Childs

Even in the utterly dry language of science, there is no way to describe the mating behavior of the sea slug Chromodoris reticulata as anything other than bizarre. The creature, native to the Pacific Ocean, engages in simultaneous hermaphroditic mating—that is, each slug has both a penis and a vagina, and when mating, both members of a couple inserts their penises into the other’s vagina at the same time—but that’s not nearly the strangest aspect of their reproduction efforts.

As discovered by a group of Japanese scientists and revealed today in the journal Biology Letters, it’s what C. reticulata does after sex that is particularly unexpected—and previously unknown in the animal kingdom. After copulating for about 10 minutes, each slug discards its penis and immediately begins growing a new one, which is ready for use within 24 hours.

Two slugs engaged in simultaneous hermaphroditic mating, each inserting a penis into the other’s vagina (center). Image via Biology Letters, Sekizawa et. al.

The slug’s discarded penis, free-floating after copulation. Image via Biology Letters, Sekizawa et. al.

The research team, led by Ayami Sekizawa of Osaka City University, gathered a number of specimens from coral reefs off of Okinawa and observed their mating behavior in lab tanks. They found that the slugs typically mated for roughly 10 minutes—with each member of a couple assuming both the female and male roles simultaneously—then disengaged, wherein their penises fell off and floated free in the water.

Within roughly 24 hours, the slugs’ penises grew back and they were able to mate once again. If they put a slug in a tank with another before that period had elapsed, it either served just a female role during copulation or avoided mating entirely.

With a full day for regeneration, though, their mating behavior was entirely regular. One particularly vigorous specimen was even able to grow its penis back twice in a row, mating 3 times consecutively with 24 hours between each instance.

The physiology that allows the slug to achieve this feat is fascinating in itself. The researchers observed that the animal’s vas deferens—the coiled internal duct that transports sperm outward—serves as a sort of “next penis” (their phrasing), extending out of the body to replace the old discarded penis.

Why would an organism go to the trouble of regenerating a new penis each time it mates? The scientists speculate that the strange behavior could be an evolutionary response to competition among mates.

The tips of the slugs’ penises, it turns out, are covered with microscopic barbs that were observed to be coated with sperm after mating. This might not be the particular slug’s sperm, the researchers theorize, but a competitor’s—and the barbs might exist to remove sperm deposited by previous slugs in their mates’ vaginas, thereby increasing the chance that it’s their sperm that leads to reproduction. Afterwards, instead of retaining a penis covered in a competitor’s sperm, it’s simpler to discard it and grow a new one.

So no matter how difficult your romantic trials and tribulations, it’s worth remembering: We still have it quite a bit easier than C. reticulata.

Image via SuperFantastic

It’s conventional wisdom that three things in life are inevitable: death, taxes and smelly armpits. But the third trouble on that list, it turns out, only afflicts 98% of us. According to a group of researchers from the University of Bristol in the UK, 2 percent of people (at least in their survey) carry a rare version of the gene ABCC11 that prevents their armpits from producing an offensive odor.

The study, published yesterday in the Journal of Investigative Dermatology, examined 6,495 British mothers who have been part of a longitudinal health study since they gave birth in either 1991 or 1992. About 2 percent—117 mothers, to be exact—had the gene, according to DNA analysis.

Researchers have apparently known that this gene exists for some time, although most work on it has focused on its connection to earwax: People with the rare gene variant are more likely to have “dry” earwax (as opposed to wet or sticky). Thus, one way to try figuring out if you’ve been blessed with stink-free armpits is to consider whether your earwax is uncommonly dry. It’s also been discovered that the non-stinky gene is more common in East Asian populations.

Researchers still aren’t sure how the gene affects both earwax and sweat odor, but they believe it has to do with amino acid production. Rapidly growing bacteria give sweat its smelliness, and people with the rare gene variant appear to produce less of an animo acid that engenders bacteria growth.

This particular study examined just how many of these remarkable individuals still wear deodorant despite their lucky genetic inheritance. Whether they knew that they carried the gene or not, people with the trait were less likely to wear deodorant or antiperspirant: 78% reported wearing it on all or most days, versus 95% of the others in the study. At some point in their lives, a decent proportion must have figured out that they really don’t need to wear these sorts of products to avoid stinking.

Still, most of the people with the gene wake up everyday and apply deodorant, a trend the researchers chalk up to socio-cultural norms. They think their findings could save these people a little money and trouble and let them skip deodorant entirely.

“These findings have some potential for using genetics in the choice of personal hygiene products,” Santio Rodriguez, the lead author, said in a statement. “A simple gene test might strengthen self-awareness and save some unnecessary purchases and chemical exposures for non-odour producers.”

A noble cause, indeed. We have just one suggestion: You may want to confirm you have the gene before leaving the house au naturale.

A new DNA analysis method reveals how ancient skeletons would have looked in the flesh. Image via Jolanta Draus-Barini, Susan Walsh, Ewelina Pospiech, Tomasz Kupiec, Henryk Glab, Wojciech Branicki and Manfred Kayser

For years, when museums, textbooks or other outlets attempted to illustrate what a particular ancient human skeleton would have looked like in the flesh, their method was admittedly unscientific—they basically had to make an educated guess.

Now, though, a group of researchers from Poland and the Netherlands has provided a remarkable new option, described in an article they published in the journal Investigative Genetics on Sunday. By adapting DNA analysis methods originally developed for forensic investigations, they’ve been able to determine the hair and eye color of humans who lived as long as 800 years ago.

The team’s method examines 24 locations in the human genome that vary between individuals and play a role in determining hair and eye color. Although this DNA degrades over time, the system is sensitive enough to generate this information from genetic samples—taken either from teeth or bones—that are several centuries old (although the most degraded samples can provide information for eye color only).

As a proof of concept, the team performed the analysis for a number of people whose eye and hair color we already know. Among others, they tested the DNA of Władysław Sikorski, a former Prime Minister of Poland who died in a 1943 plane crash, and determined that Sikorski had blue eyes and blonde hair, which correctly matches color photographs.

But the more useful application of the new method is providing new information. “This system can be used to solve historical controversies where colour photographs or other records are missing,” co-author Manfred Kayser, of Erasmus University in Rotterdam, said in a statement.

For example, in the paper, the researchers analyzed the hair and eye color for a female skeleton buried in the crypt of a Benedictine Abbey near Kraków, Poland, sometime between the 12th and 14th centuries. The skeleton had been of interest to archaeologists for some time, since male monks were typically the only people buried in the crypt. The team’s analysis showed that she had brown eyes and dark blond or brown hair.

The team is not sure yet just how old a skeleton has to be for its DNA to be degraded beyond use—the woman buried in the crypt was the oldest one tested—so it‘s conceivable that it might even work for individuals who’ve been in the ground for more than a millenium. The researchers suggest this sort of analysis could soon become part of a standard anthropological toolkit for evaluating human remains.

A new study indicates that marijuana isn’t a painkiller, but a pain distracter: Under the influence of THC, the same levels of pain are simply less bothersome. Image via Wikimedia Commons/Cannabis Training University

One of the chief arguments for the legalization of medicinal marijuana is its usefulness as a pain reliever. For many cancer and AIDS patients across the 19 states where medicinal use of the drug has been legalized, it has proven to be a valuable tool in managing chronic pain—in some cases working for patients for which conventional painkillers are ineffective.

To determine exactly how cannabis relieves pain, a group of Oxford researchers used healthy volunteers, an MRI machine and doses of THC, the active ingredient in marijuana. Their findings, published today in the journal Pain, suggest something counterintuitive: that the drug doesn’t so much reduce pain as make the same level of pain more bearable.

“Cannabis does not seem to act like a conventional pain medicine,” Michael Lee, an Oxford neuroscientist and lead author of the paper, said in a statement. “Brain imaging shows little reduction in the brain regions that code for the sensation of pain, which is what we tend to see with drugs like opiates. Instead, cannabis appears to mainly affect the emotional reaction to pain in a highly variable way.”

As part of the study, Lee and colleagues recruited 12 healthy volunteers who said they’d never used marijuana before and gave each one either a THC tablet or a placebo. Then, to trigger a consistent level of pain, they rubbed a cream on the volunteers’ legs that included 1% capsaicin, the compound found that makes chili peppers spicy; in this case, it caused a burning sensation on the skin.

When the researchers asked each person to report both the intensity and the unpleasantness of the pain—in other words, how much it physically burned and how much this level of burning bothered them—they came to the surprising finding. “We found that with THC, on average people didn’t report any change in the burn, but the pain bothered them less,” Lee said.

This indicates that marijuana doesn’t function as a pain killer as much as a pain distracter: Objectively, levels of pain remain the same for someone under the influence of THC, but it simply bothers the person less. It’s difficult to draw especially broad conclusions from a study with a sample size of just 12 participants, but the results were still surprising.

Each of the participants was also put in an MRI machine—so the researchers could try to pinpoint which areas of the brain seemed to be involved in THC’s pain relieving processes—and the results backed up the theory. Changes in brain activity due to THC involved areas such as the anterior mid-cingulate cortex, believed to be involved in the emotional aspects of pain, rather than other areas implicated in the direct physical perception of it.

Additionally, the researchers found that THC’s effectiveness in reducing the unpleasantness of pain varied greatly between individuals—another characteristic that sets it apart from typical painkillers. For some participants, it made the capsaicin cream much less bothersome, while for others, it had little effect.

The MRI scans supported this observation, too: Those more affected by the THC demonstrated more brain activity connecting their right amydala and a part of the cortex known as the primary sensorimotor area. The researchers say that this finding could perhaps be used as a diagnostic tool, indicating for which patients THC could be most effective as a pain treatment medicine.

Some reindeer really do have red noses, a result of densely packed blood vessels near the skin’s surface. Image courtesy of Kia Krarup Hansen

In 1939, illustrator and children’s book author Robert May created Rudolph the Red-Nosed Reindeer. The character was an instant hit—2.5 million copies of May’s booklet were circulated within a year—and in the coming decades, Rudolph’s song and stop-motion TV special cemented him in the canon of cherished Christmas lore.

Of course, the story was rooted in myth. But there’s actually more truth to it than most of us realize. A fraction of reindeer—the species of deer scientifically known as Rangifer tarandus, native to Arctic regions in Alaska, Canada, Greenland, Russia and Scandinavia—actually do have noses colored with a distinctive red hue.

Now, just in time for Christmas, a group of researchers from the Netherlands and Norway have systematically looked into the reason for this unusual coloration for the first time. Their study, published yesterday in the online medical journal BMJ, indicates that the color is due to an extremely dense array of blood vessels, packed into the nose in order to supply blood and regulate body temperature in extreme environments.

“These results highlight the intrinsic physiological properties of Rudolph’s legendary luminous red nose,” write the study’s authors. “[They] help to protect it from freezing during sleigh rides and to regulate the temperature of the reindeer’s brain, factors essential for flying reindeer pulling Santa Claus’s sleigh under extreme temperatures.”

Obviously, the researchers know reindeer don’t actually pull Santa Claus to deliver gifts around the world—but they do encounter a wide variation of weather conditions on an annual basis, accounting for why they might need such dense beds of capillary vessels to deliver high amounts of blood.

To come to the findings, the scientists examined the noses of two reindeer and five human volunteers with a hand-held video microscope that allowed them to see individual blood vessels and the flow of blood in real time. They discovered that the reindeer had a 25% higher concentration of blood vessels in their noses, on average.

They also put the reindeer on a treadmill and used infrared imaging to measure what parts of their bodies shed the most heat after exercise. The nose, along with the hind legs, reached temperatures as high as 75°F—relatively hot for a reindeer—indicating that one of the main functions of all this blood flow is to help regulate temperature, bringing large volumes of blood close to the surface when the animals are overheated, so its heat can radiate out into the air.

In an infrared image, a reindeer’s nose (indicated by arrow) is shown to be especially red, a reflection of its temperature-regulating function. Image via Ince et. al.

Read more articles about the holidays in our Smithsonian Holiday Guide here

The alluring memory of urinary pheromones lingers in female mice for weeks. Image courtesy of Michael Thom, University of York

It’s frequently said that scent is the sense most powerfully tied to memory. For mice, it turns out, that’s especially true—at least when it comes to a sniff of the urine of potential mates.

According to a study published today in Science by researchers from the University of Liverpool, female mice exposed to the potent pheromone darcin (found in male mouse urine) just a single time will repeatedly return to the exact site of exposure up to 14 days later, even after the pheromone is taken away.

“We have shown that a male sex pheromone in mice makes females . . .remember exactly where they encountered the pheromone and show a preference for this site for up to two weeks afterwards,” said lead author Sarah Roberts in a statement. “Given the opportunity, they will find that same place again, even if they encountered the scent only once and the scent is no longer there.”

As part of the experiment, the researchers left female house mice in a cage that had two petri dishes—one filled with water, the other with male mouse urine—for either one, two, or three ten minute periods spaced out over the course of a day. Then, 24 hours later, they put them back in the cage, with both dishes taken away.

The alluring memory of urine was remarkably potent: All the female mice demonstrated a noted preference for the spot in the cage where the urine had been. Even the mice who’d only sniffed the urine once lingered at the spot where they’d remembered smelling it roughly five times as long as where the water had been placed.

When they tested other mice who’d been exposed after waiting periods of 2, 3, 7, 10 and 14 days, they showed nearly as distinct a preference, indicating that their enticing memories of the pheromone lingered for some time. It was only after 28 days that the mice finally stopped returning to the site of the urine.

“This attraction to the place they remember is just as strong as attraction to the scent itself,” said co-author Jane Hurst. “Darcin, therefore, induces mice to learn a spatial map of the location of attractive males and their scents, to which they can easily return.”

The researchers determined that the important factor was the pheromone darcin because the same results occurred when a synthetic version of the chemical was put into a petri dish on its own. Additionally, when the female mice were exposed to female urine instead, there was no indication of a preference, because darcin isn’t present in the females’ urine.

Interestingly, the pheromone also produced a powerful effect on another group of mice: competitor males. When they were used in the same experiment, they also demonstrated a preference for the place where they remembered smelling other males’ urine, but they didn’t show this type of spatial memory when the urine used was their own. The researchers speculate that this is because of a motivation to linger near the site and mark the territory with their own pheromone scent, to advertise their availability to female mates.

The scientists speculate that this lingering affinity for the memory of urine is used by the mice as a mental shortcut for finding mates. In a natural setting (instead of cages), rather than having to smell the pheromones from a distance and then track them to the source, they can simply camp out by urine deposited by a potential mate and wait for their likely return.

Principles from the weather models that predicted Sandy a week ahead of time might be used to warn about the flu before it arrives. Image via Wikimedia Commons/CDC

Last month, despite the tragic consequences of Hurricane Sandy, one thing became apparent—the powerful weather models now available have become better and better at helping forecasters predict where storms like Sandy are going next.

That technology is more useful than just storm prediction. In a study published yesterday in the Proceedings of the National Academy of Sciences, a pair of researchers have harnessed this tech to predict the spread of influenza. With real-time data from Google Flu Trends, their models can forecast where, when and how severely seasonal flu outbreaks will occur across the country.

“[Our] findings indicate that real-time skillful predictions of peak timing can be made more than seven weeks in advance of the actual peak,” writes Jeffrey Shaman, an environmental scientist from Columbia University, and Alicia Karspeck of the National Center for Atmospheric Research, in their paper. “This work represents an initial step in the development of a statistically rigorous system for real-time forecast of seasonal influenza.” If such hopes come to fruition, there could be something like an advance flu warning system (“flu rates are projected to peak in your area next week”) similar to those for hurricanes and other severe weather events.

Both weather and flu transmission are examples of non-linear systems: ones in which a small change in starting conditions can bring about an enormous change in outcomes. In building weather models, scientists look at historical data about how these sorts of small changes (slightly warmer water in the Caribbean, say) have affected outcomes (a hurricane with much more strength when it makes landfall on the East Coast). By assimilating years of data and running countless simulations, they can generate a reasonably accurate prediction for the odds of hypothetical weather events occurring within a period of about a week.

In the new study, the researchers used principles derived from these models and applied them to the spread of the flu. For inputs, in addition to atmospheric measurements of temperature, pressure and wind, they used Google Flu Trends, a service that provides real-time data on flu transmission around the world by closely examining search terms entered into Google. While not every person searching for “flu” necessarily has influenza, Google researchers have shown that flu-related search terms can be an accurate proxy for flu transmission rates around the globe—if many people in a particular area are suddenly googling for “flu,” it’s a good bet that the infection has arrived en masse.

Influenza seems to behave according to probabilistic principles involving atmospheric conditions similar to the weather. Other factors to consider include an area’s population density. In combining factors like humidity and temperature with data from Google and actual flu rate information kept by hospitals, the researchers were able to develop models that approximate how flu has been transmitted in the years since officials have been keeping track.

To test their model, the researchers assessed New York City flu data from 2003 to 2008. By entering data on flu transmission up to a given time and asking the model to provide a weekly forecast for how the flu would behave, they were able to produce accurate forecasts of when the infection would peak, sometimes up to seven weeks ahead of time. Additionally, as with weather models, the system can distinguish between several different scenarios and provide estimates of how likely each one is to occur.

With continued development and real-time data like Google Flu Trends available, this type of technology could theoretically be put to use to generate a flu forecast for local areas, even down to the state or city level.

Scientists say the hormone ghrelin can drive us to eat high-calorie foods like desserts, even on a full stomach. Image via Flickr user browniesfordinner

It’s a gastronomic phenomenon that some call the “dessert shelf”: the remarkable ability of many a Thanksgiving eater to feel completely full after the main course, yet still have room for dessert. Of course, the ability to eat sweets on a full stomach isn’t limited to Thanksgiving, but it’s especially apparent after the holiday feast.

What makes this possible? Scientists have long known that a hormone called ghrelin, which is produced by cells lining the stomach, plays a role in inducing appetite. A counterpart hormone called leptin, which produced in fat cells and other types of tissue, suppresses appetite. When levels of ghrelin in the bloodstream are high, we feel hungry; after eating, ghrelin levels drop off and leptin levels increase, signaling to our brain that we’re full. That, anyway, is how it’s supposed to work.

However, a study involving ghrelin-deficient rats published this past summer by researchers from Carleton University in Canada suggests that something else is going on when we are confronted with sweets. Ghrelin could be leading us to eat high-calorie, high-fat foods like pumpkin pie even after our stomachs are full.

In the experiment, the researchers studied 10 normal rats and 10 rats from a special strain that lacked the gene that codes for the brain’s ghrelin receptors. For this group of knockout rats, no matter how much ghrelin their stomachs produced, the brain had no way of registering the hormone and registering that the rat was hungry.

For four days in a row, the researchers gave all of the rats access to standard-grade rat food from 10 a.m. to 2 p.m. Both groups of rats ate roughly the same amount of food, which provided enough calories to give them sufficient energy to go about their day.

On the fifth day, though, after the rats ate their standard meal, the researchers gave them an unexpected treat: a 30-gram ball of cookie dough. Since the average lab rat is roughly 700 grams at maturity, that’s the equivalent of giving a 125-pound person a ball of cookie dough over 5 pounds in weight.

As you might expect, both groups of rats ate some cookie dough. But at least among this small sample, the normal rats—those whose brains could be affected by ghrelin—ate a fair amount more: 8 grams of cookie dough, on average, compared with the 6 grams the knockout rats ate. This 2-gram difference might not seem like much, but in terms of the rats’ size, it’s significant—roughly the difference between a person eating 1.5 pounds of cookie dough, instead of just a little over a pound.

Ghrelin doesn’t completely explain why we’re able to eat dessert after feeling full—but it seems to play a role. “This result supports the idea that ghrelin is involved in reward-based feeding and delays the termination of a meal,” Veronique St-Onge, a Ph.D. candidate at Carleton University and the lead author the paper, said in a statement. It was the persistent influence of ghrelin, she and coauthor Alfonso Abizaid speculate, that led the already-full rats to eat even more cookie dough.

Other research has looked at the role of ghrelin in stimulating stress-based eating. In one study, normal rats exposed to a stressful situation gravitated towards high-calorie, high-fat food, while the special rats without ghrelin receptors did not, suggesting that the hormone could act as something like an antidepressant, enabling the brain to use food as a reward after a period of anxiety. Another study has even implicated the hormone in alcoholism and the excessive consumption of other drugs as well.

So on Thanksgiving, when the main course is over and you find yourself with room for dessert, blame (or maybe give thanks for) ghrelin.

Illacme plenipes, the record-breaking millipede, only lives in a few woodlands in Northern California. Image via Marek et. al.

Yesterday, the first full description of the species was published in the joural ZooKeys. The study was led by Paul Marek of the University of Arizona. The millipede is known only from 17 live specimens Marek’s team found in a home range that is remarkably specific: three small wooded areas strewn with Arkose sandstone boulders in the foothills of San Benito County, California, near San Francisco.

The rareness of the millipede meant that from 1928 until 2005—when Marek, then a Ph.D. student, found a few specimens in the woods near San Juan Bautista—most scientists had simply assumed the species had gone extinct. Over the past seven years, Marek and his colleagues have taken several trips to the area, typically searching for hours before finding a single specimen clinging to the side of a boulder or tunneling four to six inches down into the ground.

In studying these specimens under a microscope, Marek has discovered a number of surprising characteristics that go beyond its legs. ”It basically looks like a thread,” Marek told LiveScience. “It has an uninteresting outward appearance, but when we looked at it with SEM [scanning electron microscopes] and compound microscopes, we found a huge, amazingly complex anatomy.”

The new analysis revealed that the millipede has no eyes, disproportionately long antennae and a rudimentary fused mouth adapted for sucking and piercing plant structures. It also has specialized body hairs on its back that produce silk, which may be used as a defense mechanism to clear bacteria off the millipedes’ bodies.

A microscope image of the species’ specialized body hairs that produce a silk secretion. Image via Marek et. al.

Of course, the legs are the most striking part of the species’ anatomy. Despite the name millipede, no species are known to have 1,000 legs, but Illacme plenipes comes closest (its Latin name actually means “in highest fulfillment of feet”). The male specimens examined had at most 562 legs, but the females had more, with the winner at 750.

Most millipedes have somewhere between 80 and 100 legs. Marek and his colleagues speculate that this species’ extreme legginess could be a beneficial adaptation for subterranean tunneling or even for clinging to the boulders widely found in the species’ habitat.

Most millipedes have 80 to 100 legs, but this species has up to 750. Image via Marek et. al.

DNA analysis has revealed that its closest cousin, Nematozonium filum, lives in Africa, with the two species’ ancestors apparently splitting apart sometime soon after the breakup of Pangea, more than 200 million years ago.

The team has tried to grow the millipedes in a lab but has so far been unable to. They caution that the species could be extremely endangered—in 2007, they stopped searching for wild specimens out of fears that they were depleting the population—and advocate for a formal protection listing, so scientists will have the time to learn more about them before the millipedes go extinct.