Author: Kate Horowitz

In a move hailed by conservationists, an international governing body has created the world’s largest marine protected area in the Ross Sea. The designation will protect 598,000 square miles of water off the Antarctic coast, a region teeming with wildlife from krill to killer whales.

The Commission for the Conservation of Antarctic Marine Living Resources (CCAMLR) was created by international convention in 1982 and includes delegates from 24 countries, including the United States, and the European Union. The commission was founded in response to growing commercial fishing interest in Antarctic krill—an essential link in the marine food chain.

Both krill and plankton are abundant in the near-pristine Ross Sea. Their presence provides food for the tiniest sea creatures, which in turn are eaten by little animals, onward and upward all the way to pods of minke and killer whales.

“The Ross Sea is probably the largest ocean wilderness left on our planet,” marine biologist Enric Sala told National Geographic. “It is the Serengeti of Antarctica, a wild place full of wildlife such as emperor penguins, leopard seals, minke whales, and killer whales. It’s one of these rare places where humans are only visitors and large animals rule.”

The sea’s isolation kept it safe for a long time. But as commercial interests enlarge and fuel prices drop, even these frigid waters will need more official forms of protection.

The new ruling prohibits fishing in 72 percent of the reserve, while other areas will be open to limited collections for scientific purposes. “A number of details regarding the MPA are yet to be finalized but the establishment of the protected zone is in no doubt and we are incredibly proud to have reached this point,” Andrew Wright, CCAMLR executive secretary, said in a statement.

Protections will go into effect in December 2017 and hold for 35 years. It’s a very welcome development, say conservationists, but it’s also a temporary fix.

Rod Downie is the polar program manager for the World Wildlife Fund. “This is a milestone for the conservation of Antarctica and the Southern Ocean,” he told New Scientist. “We want a permanent and enduring agreement for future generations that will safeguard the whales, penguins, seals and thousands of other amazing species that live there.”
 
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Some of the most powerful human experiences are universal. Love. Heartbreak. Elation. Hating acne. The microscopic jerk known as Propionibacterium acnes wreaks havoc on our skin, makes middle school harder, and can cause pain and scarring. Now scientists say we’re one step closer to understanding what makes acne so devious—and how we might conquer it. They published their findings in the journal Science Immunology.

Acne breakouts are the result of a perfect storm of disgusting conditions near the surface of your skin. Natural oils and dead cells build up around your hair follicles, creating the ideal environment for bacteria to breed. The resulting infection sets off your immune system, which leads to inflammation, redness, and those oh-so-delightful pustules on your face, neck, chest, back, or shoulders.

We knew all this already. What we didn’t know was how P. acnes, which ordinarily lives harmlessly on the skin, could multiply out of control—or how its little fortresses in your follicles send your immune system into such a panic.

Previous studies on the bacteria in the human gut have found that certain bacteria produce chemicals called short-chain fatty acids (SCFAs). These acids then block the action of an immune compound called histone deacetylase (HDAC). Suppressed HDAC can then lead to immune trouble and, from there, inflammation.

Dermatology and biochemists at the University of California, San Diego were curious to see if the same patterns would play out on and inside our skin. First, they simulated the greasy skin experience by culturing acne bacteria in Petri dishes full of blood cells or oil-producing skin cells. They ensured that the environment in the dish was smothering, starved of oxygen like the inside of a clogged follicle. Then they let it fester.

Once they had a good SCFA stew going, they ran the cultures through an RNA sequencer to see how the bacteria and cells were performing. They also applied SCFAs both on and just under the skin of lab mice to see how skin layers might react.

The team found that, as with gut cells, the skin cells could be goaded into inflammation by acne’s SCFA bullies. The same pattern bore out for the mice—but only on the topmost layer of keratinocytes, the most common type of epidermal cells. Exposing lower skin layers to acne and SCFA actually activated those cells’ immune systems, making it easier for them to fight off infection.

Adam Friedman teaches and researches dermatology at the George Washington University School of Medicine. He was unaffiliated with the study but praised the findings, telling mental_floss that they “unveil a new understanding of how P. acnes contributes to the pathogenesis of acne, but also give us more insight (and also much more work to do) with respect to the way the bacteria on our skin can change how skin works at the genetic level.”

The research goes well beyond skin problems, he says, and has “huge implications for microbiome research,” because it highlights how “our many tiny friends who live on our skin have the ability to modify how we work, which has broader implications for other inflammatory diseases.”
 
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Researchers may have found something extraordinary inside a plain-looking pebble: fossilized dinosaur brain. They described their findings [PDF] in a special publication from the Geological Society of London. 

Twelve years ago, fossil hunter and paper co-author Jamie Hiscocks was looking through an exposed sandstone riverbed in Sussex, England, when he spotted a round brown stone. Hiscocks brought the rock to the attention of renowned paleobiologist Martin Brasier at the University of Cambridge. The two men immediately began speculating on the rock’s contents.

“I noticed there was something odd about the preservation,” Hiscocks said in a statement, “and soft tissue preservation did go through my mind. Martin realized its potential significance right at the beginning.”

Brasier and colleagues at the University of Cambridge and the University of Western Australia began exploring the mysterious rock from every imaginable angle. They put it through a computed tomography (CT) scanner to look inside and examined its smallest details using super-high-powered microscopes.

What they found astounded them. The nondescript-looking rock, they say, concealed the remains of some prehistoric animal’s brain. Close-up images revealed fragments from the supportive membrane surrounding the brain, plus blood vessels and cortices from within.

The team believes the brain may have belonged to an iguanodon-like dinosaur that lived in the Early Cretaceous period around 133 million years ago. The fact that the chunk of brain has lasted this long is “astonishing,” said co-author Alex Liu.

The researchers say the brain’s owner likely met its demise in or near a body of water. It probably then became at least partially submerged and buried in sediment at the bottom, where acidic water and a lack of oxygen helped preserve the tissue.

“As we can’t see the lobes of the brain itself, we can’t say for sure how big this dinosaur’s brain was,” co-author David Norman said. “What’s truly remarkable is that conditions were just right in order to allow preservation of the brain tissue—hopefully this is the first of many such discoveries.”

However, some paleontologists are reserving judgment about the fossil until further research is done, including the American Museum of Natural History’s Mark Norell, who told NPR he is “not convinced” the find is a dinosaur brain.

Martin Brasier did not live to see the results of this research, but the team’s report on their findings was published in a special volume dedicated to his life and work.
 
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Today in “You Guys, The Ocean Is So Weird”: Scientists say some crustaceans wear mattifying living layers to hide from predators. A report on the sea critters’ clever camo was published in the journal Current Biology.

Amphipods are a group of shrimplike crustaceans that make their homes in a variety of venues, from freshwater to beaches and deep into the sea. They’re not particularly charismatic creatures, but charisma doesn’t count for much in the darkness of the ocean. What counts is adaptability.

Some species have developed glowing fishing poles; others, sparkling arms. Some creatures light up in order to be seen, while others use illumination to hide. Others, like these amphipods, would prefer to avoid light altogether.

This is harder for them than it would be for you or me. Why? Because they’re naturally transparent—and reflective.

Scientists put seven specimens of mid-water amphipod species under high-powered microscopes and looked closely at their shells. When they zoomed way in, they discovered that all the amphipods were sporting little coats of what looked like beads on their bodies and legs. The beads themselves are microscopic, ranging from 50 to 300 nanometers in diameter depending on the species. This makes them just the right size and shape for absorbing undersea light.

 
Biologist Laura Bagge is lead author on the study and a Ph.D. candidate at Duke University. Speaking in a press statement, she said the coating reduces reflections “the same way putting a shag carpet on the walls of a recording studio would soften echoes.” Some species’ coatings could cut down on glare by as much as 250-fold, rendering them effectively invisible to wide-eyed predators.

The coats are certainly effective. But what are they?

We’re not totally sure. “They have all the features of bacteria,” Bagge said, “but to be 100 percent sure, we’re going to have to perform an in-depth sequencing project.”

Crustaceans shed their shells on a regular basis. For carefully camouflaged amphipods, this could mean becoming shiny again—unless they take their special coats with them. If the mattifying layers are indeed made of bacteria, they could easily be transferred to a new shell as the amphipod tugs its way out of the old one.

 
They could also share them with their kids. Phronima amphipods raise their babies in the hollowed-out bodies of a translucent creature called a salp. The researchers say it would be pretty simple for a mama amphipod to pass her coating materials on to little ones in the nest.
 
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Happy Bat Week! If you’ve already hung up your bat-themed garlands and are looking for other ways to celebrate, we’ve got you covered with two brand-new live streams of vampire and fruit bats at the Cranbrook Institute of Science.

Bats are important contributors to our planet. In addition to eating tons of disease-carrying mosquitoes and other bugs, they also pollinate plants—including agave, without which we wouldn’t have tequila. (So, thank a bat for that margarita.)

Many bats are small and fluffy. Some tilt their heads like puppies when hunting bugs. Some even sing to their mates. If none of this has convinced you that bats are great, then head right to the video and see them for yourself.

Tip: Unlike wild bats, the ones at Cranbrook are diurnal, which means it’ll be more fun to watch them during the day.

The fruit bat colony includes a Malayan flying fox, straw-colored fruit bats, and Egyptian fruit bats:

And your classic vampire bats:

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The global spread of AIDS was one of the greatest public health crises of the last century. While we’ve made tremendous advances in human immunodeficiency virus (HIV) prevention and treatment, the details of the virus’s global spread have been harder to pin down. A new report published this week in Nature sheds light on when and where HIV arrived in the United States: in New York City around 1970. It also removes blame from the man long known as “Patient Zero”—he was not, in fact, the first person in North America to contract the virus.

Because HIV attacks the immune system, limiting the body’s ability to fight infections or infection-related cancers, the first patients presented with a range of symptoms, from enlarged lymph nodes and pneumonia to cancer. Physicians in California first recognized it as a single entity in 1981, but the disease didn’t get a name—acquired immunodeficiency syndrome (AIDS)—until a year later. By then, media reports of a “gay cancer” had begun to raise alarms and stigma across the country. The first drugs to treat HIV were not approved until 1987, by which time the disease had taken more than 40,000 lives.

Part of the problem lay in the limitations of medical and scientific technology. We didn’t have the capability to look inside the disease with the level of detail required to stop it. Blood tests could pick up on the presence of HIV in a sample, but they couldn’t spell out its genetic code. To do that, said study co-author and virus evolution expert Michael Worobey of the University of Arizona, researchers would need a sample of RNA from the virus itself—a serious challenge, as the virus’s RNA is super delicate and breaks down at the slightest provocation.

But we’ve come a long way since then. Worobey and his colleagues in Arizona and at the University of Cambridge have created a vividly named new technique called RNA jackhammering that allows them to break down the human genes in a blood sample and extract and examine the virus RNA hiding within them.

To rewind the clock to HIV’s early days in the States, the researchers applied their jackhammers to blood samples taken from more than 2000 men in New York and San Francisco in 1978 and 1979. The nearly 40-year-old samples had degraded since their collection, but Worobey and his colleagues were still able to extract eight near-complete HIV RNA sequences, creating the oldest-known record of North American HIV genetics.

By comparing these sequences with those collected from other parts of the globe, the researchers were able to trace the virus’s evolution and devastating spread. They found that HIV had crossed from Africa to the Caribbean, and from there jumped to New York City and then San Francisco, where the first patients were identified. These findings run counter to earlier theories, which pinpointed the virus’s U.S. landfall to San Francisco.

The density of vulnerable populations in New York City were like “dry tinder” for HIV, Worobey said in a press statement, “causing the epidemic to burn hotter and faster and infecting enough people that it grabs the world’s attention for the first time.”

By the time the blood samples were collected, the authors say, the virus had already evolved into the form it bears today.

Their analysis also upends another well-known element of the AIDS story: the identity of “Patient Zero.” For nearly three decades, scientists have traced the virus’s entry to the U.S. back to one man: Gaëtan Dugas. But Worobey and his colleagues tested a sample of Dugas’s blood from 1983 and found that the virus RNA in his blood was no less evolved—and therefore no older—than the viral genes in his peers. He wasn’t Patient Zero.

That the weight of the AIDS pandemic ever came to be placed on Dugas’s shoulders at all may itself have been a simple typographical error, the authors write. The man’s original file identified him as a patient from Outside of California, or Patient O. Somewhere along the way, the letter O became a zero, a mistake that would be perpetuated for decades—long after Dugas himself had died.

The authors are hopeful that their findings and their new technique will help accelerate scientific unraveling of the virus.

“Earlier detection and better alignment of the various options we have to make it harder for the virus to move from one person to the next,” Worobey said, “are key to driving HIV out of business.”
 

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Dating sucks. There’s no two ways about it. It sucks even more if you’re a backward snail—unless you happen to have some very dedicated friends. Scientists at the University of Nottingham are asking the public to help them find a very special date for Jeremy the garden snail, whose unique anatomy has so far made mating impossible.

Most garden snails are dextral—that is, their shells spiral to the right, and the rest of their anatomy follows suit. This works out for them when it comes time to get busy; snails are hermaphroditic, possessing both sperm transmitters and receptacles. They mate by lining up face-to-tail like a slow-moving yin-yang, then exchanging fluids. (Fair warning: this is a lot less cute than it sounds. There are projectiles involved.)

In order for this to work, each snail’s part must line up with its partner’s relevant regions. They find each other in the wild and all get down to it.

Well, all except for Jeremy, who was found on a Nottingham compost heap by a former biologist. Jeremy’s body is a mirror image of the average snail’s. His* shell curls to the left, and his parts don’t line up with anyone’s.

To Angus Davison and other snail researchers at the university, Jeremy’s predicament is more than just a sad situation. It’s an opportunity.

“I have been studying snails for more than 20 years, and I have never seen one of these before,” Davison said in a statement. “We are very keen to study the snail’s genetics to find out whether this is a result of a developmental glitch or whether this is a genuine inherited genetic trait.”

Davison has good reason to suspect Jeremy is genetically different. In a study published in February of 2016, Davison and his colleagues reported finding the gene associated with snail-shell spiral direction. They found that the same gene, called Formin, may also affect laterality (sidedness) in frogs and other vertebrates.

The best way to learn about Jeremy’s genes would be to examine his descendants. But, as previously discussed, Jeremy has none.

It’s not that snails can’t reproduce asexually, Davison says. They just don’t like it. “And from our perspective, the genetic data from offspring of two lefty snails would be far richer and more valuable to us.”

Which is where we come in. Davison and his colleagues are hoping to crowd-source a date for Jeremy. They’re asking snail lovers to keep an eye out for another lefty snail—the yin to Jeremy’s yang.

If the sheer generous pleasure of helping a mollusk find a mate is not enough for you, Davison is willing to sweeten the pot with a taste of fame. “There is a chance, because it is such a rare thing, that anyone who can find and identify another one of these snails may even find themselves named as a contributor on a research paper we publish in the future.”

So: keep your eyes peeled. If you think you’ve found one, you can email Davison directly at angus.davison@nottingham.ac.uk, or Tweet your discovery using the hashtag #snaillove.

*Jeremy’s researcher friends use he/him/his pronouns despite the snail’s obvious assemblage of genitalia.
 
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It starts with a little lie—that haircut is perfect for you!—but before you know it, you’re bragging about your Olympic gold medal in curling. Now scientists at University College London and Duke University say they’ve figured out why we so naturally progress from little white lies to whoppers. They published their findings [PDF] in the journal Nature Neuroscience.

Researchers recruited 80 people between the ages of 18 and 65 and brought them into the lab to play a game. Each participant was introduced to their “partner” (actually a researcher), and then some of them were hooked up to an MRI scanner before they started playing. The premise was simple. A participant was shown a clear image of a jar of pennies. They were told that they were responsible for reporting the number of pennies to their partner via a microphone, and that their partner would pass on that information to the researchers. Both participants would then be given a certain amount of money. All participants had reason to believe that their imaginary partners were oblivious and would trust whatever they said. In some scenarios, the participants were told that the more accurate and truthful their guess, the more money they’d make. In others, they were told that they’d make more money if their partners guessed wrong; in other words, they were encouraged to lie.

The tests were set up to create four situations: those in which lying benefited both the participant and their partner; those in which it benefited only the partner; those in which it benefited only the participant; and those in which lying would only hurt them both.

The researchers noticed two clear, if unsurprising trends. First, they saw that participants’ willingness to lie increased as the game went on. Fudging a number and increasing or decreasing the estimate by a few pennies turned into a few more pennies, then a few more. Second, the tests showed that lying only increased for the two situations that benefited the participants, whether with or without their partners.

Reviewing the brain scans, the researchers could actually watch as participants became accustomed to lying. As the initial fib was taking place, the participants’ brains showed activation in the amygdala and other regions associated with strong emotional responses. It’s as if their brains were saying, “This is not a good idea. Let’s not do this.” But the next lie induced less amygdala activation, and the one after that, less still. It was as though they’d built up a tolerance to dishonesty.

Study co-author Tali Sharot compared the experience of lying to wearing a new perfume. At first, she said, the new scent is overpowering. The second time you wear it, it’s simply strong. But “two months from now when you put on the perfume,” she said in a press conference, “you can’t even smell it yourself, so you feel you have to put quite a lot on, and other people turn away. And that’s because the neurons in your olfactory bulb adapt.”

Like our sense of smell, the authors say, each person’s lying profile was different. Some participants lied more than others, and some people’s lies escalated more quickly.

The researchers have not conclusively proven that reduced amygdala activation reduces our pangs of guilt, thereby greasing the slippery slope, but they think it’s pretty likely. “This is in line with suggestions that our amygdala signals aversion to acts that we consider wrong or immoral,” said co-author Neil Garrett. “We only tested dishonesty in this experiment, but the same principle may also apply to escalations in other actions such as risk taking or violent behavior.”
 
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Picture this: you’re driving somewhere you’ve never been before, blasting your favorite tunes. As you approach your destination and start checking house numbers, your hand reaches for the dial and turns the radio down. Without even realizing it, you’ve decided to redirect your attention from sounds to sights. Now imagine that your passenger has interfered. They’ve turned the radio all the way up and opened all the windows, filling the car with the roar of traffic and wind as you’re trying to focus. Harder now, isn’t it? And it isn’t just us; scientists say mongooses exposed to traffic noise overlook crucial clues from their other senses—clues that could mean the difference between life and death. Their findings were published today in the journal Current Biology.

We’ve known for a long time that pollution and urbanization are bad news for everyone. Much of our research has focused on the physical effects like smog, water contamination, and habitat destruction. We haven’t paid too much attention to the toxic effects of too much noise until recently, but what we’ve learned is troubling.

Studies have shown that exposure to anthropogenic, or human-made, noise causes intense stress for animals, can interfere with their communication, and may even keep them from migrating and having sex. All of these issues could mess with a species’ chances of survival in the long run.

The short-term effects have been less understood, says biologist Amy Morris-Drake of the University of Bristol. She and her colleagues decided to test the immediate consequences of noise on one species, the dwarf mongoose (Helogale parvula), whose South African habitat is increasingly bounded by cities and roads.

The dwarf mongoose has many predators, including jackals, hyenas, civets, servals, honey badgers, wildcats, bigger mongooses, and an assortment of reptiles. The key to survival, consequently, is constant olfactory vigilance: sniffing the air for the scent of predator poop.

The research team headed into mongoose territory with audio recordings of traffic noise and Ziploc baggies of poop from servals, wildcats, and giraffes. (Because giraffes present no threat to mongooses, their poop was used as a control group.) The researchers set out the poop and played their road sounds, watching the mongooses to see how they would respond.

The results were not encouraging. Exposure to traffic noises significantly decreased the mongooses’ vigilance. They spent less time investigating the predator poop; they were less likely to scan the area for potential threats; and they were less likely to retreat to the entrance of their burrow to prepare for an attack. If the scientist-provided poop, and therefore the threat, had been real, those mongooses would have found themselves in significant danger.

“Our study suggests that noise pollution can have a negative effect in terms of information use,” said co-author Andy Radford. “Given the demonstrated effects, considering the interactions among multiple sensory channels is critically important if we are to understand fully the consequences of human-induced environmental change.”
 
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They’re unpleasant. They’re uncooperative. And they’re unwilling to share.* Testosterone-fueled bad behavior is as common in meerkats as it is among other animals. But there’s one major difference: In meerkat society, scientists say, it’s the females doing the misbehaving. A report on their misconduct, and its implications for their health, was published in the journal Scientific Reports.

Meerkats are intensely social animals. They live in tight-knit groups of up to 40 or 50 animals and do everything collectively, from hunting and sleeping to raising pups. They maintain order through a strict hierarchy led by a fierce matriarch and her subordinates. Meerkat matriarchs are notoriously self-involved, but other females are not much sweeter. They, and not the males, are the growlers, the biters, the brawlers, the food-swipers, and the warmongers—all identities traditionally associated with high levels of testosterone.

To find out if the females’ bad attitudes were linked to this so-called male hormone, researchers collected blood and poop samples from 93 wild meerkat males and 91 females on the Kuruman River Reserve in South Africa. The meerkats there are habituated to scientists, which made it no big deal for the team to catch them, anesthetize them, and take a little blood. They’re also clearly tagged with individual dye markings, which made it easier for the researchers to tell who was chasing (or being chased by) whom.

 
As anticipated, the blood tests showed a stark difference in hormone levels between male and female meerkats. The females’ blood boasted much more testosterone than the males’ blood did—in some cases almost double. Levels of testosterone and related hormones in females were closely linked with their place in the hierarchy. This was less true for males, whose hormones were more likely to fluctuate during mating periods.

A testosterone-charged life doesn’t come without its costs. For meerkats, as with other animals, this may mean a compromised immune system. They combed through the meerkats’ feces and counted the number of parasite eggs they found in each sample. The higher a female’s testosterone level, the higher her parasite count—and the weaker her immune response.

Riding high on testosterone may not make a lady meerkat popular, and it may not make her healthier, but all that jerk behavior could just give her—and her kids—a competitive edge.

*National Geographic appears to have gone for a slightly different tagline.
 
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