Rising carbon dioxide levels in our atmosphere are changing Earth’s climate at an unprecedented rate. Not only is our planet getting warmer on average—in the oceans, a chemical reaction spurred by dissolved CO2 is altering water chemistry, causing a decrease in pH. This effect of climate change, called ocean acidification, can dissolve the calcium carbonate foundations of coral reefs and other calcifying organisms, making it impossible to build and maintain healthy reefs. Luckily, recent studies on how corals react to lower pHs has given scientists hope that they may be more resilient than previously thought. However, to truly understand how reefs will respond to climate change, we have to look at more than just corals.
Reefs are complex ecosystems, the bases of which are comprised of so much more than corals. There are other species which act as calcifiers, adding to the carbonate foundation (such as crustose coralline algae). The contribution of these non-coral species to reef growth, called secondary accretion, helps shape the surface and guide the settlement of larval corals. There are also species that eat away at the reef, including many worms and sponges. These bioeroders can weaken reef structures until they crumble apart. Whether a reef grows or shrinks over time depends on the interplay between its corals, other reef-builders, and the burrowing organisms which eat their way through the reef’s carbonate foundation. Read More
When you look one of these little snakes in its adorable little face, it’s not hard to see how the hognose got its name. Their upturned snoots give the snakes a porcine appearance.
But hognoses don’t just have adorable nasal features—they are also the drama queens of the serpent world. If you thought William Shatner wins the prize for worst over-actor on the planet, think again:
The end in particular just slays me: “No, I’m dead. See? I’m dead. So dead. Belly up dead.” Read More
The moment a viper’s venom enters the body, its enzymatic components set about their nefarious work. Metalloproteases begin the assault by mowing down structurally essential components of blood vessels and tissues, weakening walls and making holes that leech fluid. Capillaries hemmorrhage and the area swells while the proteases keep at their attack, taking out skeletal muscle through mechanisms poorly understood. Phospholipases join in, with their sights set on cell membranes. Some cut apart membrane lipids making lethal holes, while others seem to be just as destructive without enzymatic activity. The end result: muscle tissue dies. Hyaluronidases and serine proteases aid in the efforts, and the helpless tissue succumbs to the venom’s siege.
And that’s not even the worst part. The metalloproteases and phospholipases have other tricks up their sleeves. They don’t just fight their own war on our flesh: they enlist our own immune system to help them do it. The liberation of tumor necrosis factor and immune-stimulating cytokines by metalloproteases and the release of bioactive lipids by phospholipases cause immune cells to rush to the wound. Our body’s forces are trained to kill, usually setting their sights on bacteria and viruses. But without those clear targets, the body’s army gets confused. They can’t tell friend from foe, yet the immune cells fire anyway, blindly attacking an unseen danger. Valiant volleys act as friendly fire, adding to the death toll of innocent tissues.
Though scientists have been warning about the disastrous impacts that climate change will have on our planet for decades, we are now starting to feel those predictions manifest. As Eric Holthaus pointed out, the “worst nightmare” scenarios are already happening. Droughts, storms, fires, you name it—the world as we knew it is under siege. Heck, we just had the most abnormally hot month on record; February 2016 was 1.35 degrees Celsius warmer than the average, making it two-tenths of a degree more unusually warm than the previous record month: January 2016.
And as water supplies dwindle, rainforests burn, and corals bleach, we may have yet another thing to worry about: frickin’ snakes.
Many know Neil deGrasse Tyson for his pithy, humorous science tweets, which are a part of his greater science communication strategy. As of late, though, scientists have become quite vexed with NDT’s 140-character stylings, as he’s been foraying outside his planetary expertise and into biological phenomena, getting the facts wrong every time. First, there was his mistaken evaluation of evolutionary drivers and how sex works, excellently torn apart by Emily Willingham (a Ph.D. scientist whom Tyson then condescendingly called “a woman who has a blog”, prompting some to suggest he be referred to as just a “man with a twitter”). Then came his misunderstanding of genetics and deleterious alleles, which was ripped apart by Jeremy Yoder (another Ph.D. scientist). Now, he’s stepped in guano again with this tweet related to this weekend’s powerhouse movie release:
If Batman wants so badly to be a bat, he might be more intriguing if (like Marvel’s Daredevil) he were also blind, like a Bat
— Neil deGrasse Tyson (@neiltyson) March 25, 2016
Alas, the phrase “blind as a bat” is simply wrong. Let me explain why:
It’s official: Lee Se-dol has lost his first two Go games against AlphaGo, the computer program from Google’s DeepMind. Going into the match, Lee said he was confident, predicting victory in all 5 games. So when he lost the first game, he was shellshocked: “I didn’t expect to lose,” he said.”Even when I was behind, I still didn’t imagine that I’d lose. I didn’t think that it would be able to play such an excellent game.”
He’s now 0-2 out of 5 against AlphaGo, with $1 million on the line.
As Lee sat in front of the press after the second loss, he looked visibly shaken. “Yesterday I was surprised but today it’s more than that — I am speechless,” he said. Lee rocked back and forth slightly while DeepMind founder Demis Hassabis described the program’s confidence through the game, fidgeting as the cameras snapped hundreds of photos. He has a day to think about his strategy before game 3 on Saturday
I can understand how for some, a person losing a board game to a computer might seem inconsequential; after all, the best minds in Chess were beaten by computers decades ago. But this isn’t Chess. Go, a roughly 3,000 year old game (called as weiqi in China, igo in Japan, and baduk in Korea), is staggeringly more complex than other strategy board games. It’s estimated that there are some 10761 possible games of Go (compared with 10120 for Chess)—more than the number of atoms in the known universe. This means that even the most powerful computers on the planet can’t calculate ahead to conclusively determine the best move to play. Human players rely on a mix of skill, instinct, and imagination.
I know quite well how much of a challenge it is to program a machine to mimic the art of play. After all, my dad wrote the first commercial Go program. Read More
If the above photo makes you cringe, you’re not alone. The fear of these beasts, called arachnophobia, is surprisingly common. Somewhere between 15 and 55 percent of people get anxious around spiders or even pictures of spiders. Even many who can stomach the sight of these eight-legged animals would be hesitant to perform the a brazen act of actually holding one—after all, everyone knows spider bites fester into giant, gaping sores which leave hideous scars.
At least, that’s what we grow up believing. In reality, though, there are some 40,000 species of spiders, only a dozen or so are actually dangerous to humans. And of those, only the venom of recluse spiders can cause the kind of tissue death (called necrosis) that we so often attribute to spider bites. Recent studies have shown that, instead, people assume the worst of innocent spiders when much more sinister species, such as methicillin-resistant Staphylococcus aureus (MRSA) are to blame for their wounds.
We would hope that doctors would be more discerning—that they would be able to properly identify spider bites when they (very rarely) occur. But a new paper suggests that our trusted physicians may not be better than the rest of us. A review of clinical literature found that a whopping 78% of “spider bite” cases may be misattributed. Read More
Back in 2007, a landmark paper in Science changed how everyone thought about cownose rays. These smiley aquarium ambassadors suddenly became the most hated fish in the Atlantic. As the press release for that paper stated:
A team of Canadian and American ecologists, led by world-renowned fisheries biologist Ransom Myers at Dalhousie University, has found that overfishing the largest predatory sharks, such as the bull, great white, dusky, and hammerhead sharks, along the Atlantic Coast of the United States has led to an explosion of their ray, skate, and small shark prey species.
“With fewer sharks around, the species they prey upon — like cownose rays — have increased in numbers, and in turn, hordes of cownose rays dining on bay scallops, have wiped the scallops out,” says co-author Julia Baum of Dalhousie.
The study, which described the evidence for a shark-ray-shellfish trophic cascade leading to a collapse of the Chesapeake Bay scallop fishery, became an instant classic. “This is the first published field experiment to demonstrate that the loss of sharks is cascading through ocean ecosystems and inflicting collateral damage on food fisheries such as scallops,” said Ellen Pikitch, then a professor at the University of Miami Rosenstiel School of Marine and Atmospheric Science and executive director of the Pew Institute for Ocean Science, in the original press release.
The study had all the ideal components of blockbuster research: it was led by one of the world’s most preeminent fisheries biologists. It played to both sides of an age-old rivalry; it had a strong shark conservation message, providing much needed data to support the claim that sharks are vital ecosystem components. Yet at the same time, the study hit home with locals and fishermen, explaining why a once lucrative fishery was reduced to a mere shell of its former glory. The phenomenon it described—a top-down trophic cascade, with sharks as the key species—had been hypothesized for years but never demonstrated. And, whether intended or not, the paper provided an easy and achievable solution for the area’s woes: fish the rays instead of the sharks, and everyone wins. Frankly, it just made sense.
“People thought ‘Finally! Some evidence for this top down control by sharks,’ and accepted it without critically reading and reviewing the paper,” said Dean Grubbs, an elasmobranch ecologist with Florida State University. Though Grubbs and others had issues with the paper’s methods and conclusions, especially regarding the reproductive biology of rays, their initial worries were drowned out by the loud trumpeting the paper received. “We were concerned that this could quickly get out of hand,” Grubbs said. And it did. The paper became one of the most well known studies ever conducted in marine ecology, garnering almost 900 citations in the last 9 years.
“It just seems like virtually everyone who wants to talk about shark conservation knows this story, and most of them believe it,” said Sonja Fordham, founder and president of the non-profit Shark Advocates International. But when she read the press release almost a decade ago, she remembers being “troubled” by the reference to “hordes” of cownose rays. Rays, after all, are just flattened sharks, and share many of the same life history characteristics that make sharks so vulnerable to overfishing in the first place. “The paper was very pro shark conservation, so I found it very surprising that it would not see the potential danger of suggesting that a different type of elasmobranch had run amok.”
Her worst fears were soon realized, as cownose rays became touted as sustainable seafood. The states where the rays are native, including Maryland and Virginia, pushed to put ray fillets on everyone’s plates. “As this fishery developed and this paper became more and more widely cited, we decided we had to put a rebuttal together,” said Grubbs. That rebuttal was published last week in Scientific Reports, and it tears the notion of a shark-ray-shellfish trophic cascade to shreds. Read More
It was the moment of truth.
I couldn’t believe I’d actually found it. When John Holliday told me where to look to find the infamous Dictyophora species, I didn’t really believe him—probably because he also claimed this mushroom had some pretty implausible properties. But it was there all the same, right where he said it would be. Countless hours of research and reporting had culminated in this moment. There I was, standing on the remains of an old lava flow, staring at a mushroom that one man claimed could make me orgasm by smell alone.
I bent down, pressing my hands in the soft mulch on either side of the fungus, and let the air out of my lungs. Then I pushed my face next to its orange stalk and breathed in as deeply as I could.
A new ridiculous rumor is spreading around the internets. According to conspiracy theorists, the recent outbreak of Zika can be blamed on the British biotech company Oxitec, which some are saying even intentionally caused the disease as a form of ethnic cleansing or population control. The articles all cite a lone Redditor who proposed the connection on January 25th to the Conspiracy subreddit. “There are no biological free lunches,” says one commenter on the idea. “Releasing genetically altered species into the environment could have disastrous consequences” another added. “Maybe that’s what some entities want to happen…?”
For some reason, it’s been one of those months where random nonsense suddenly hits mainstream. Here are the facts: there’s no evidence whatsoever to support this conspiracy theory, or any of the other bizarre, anti-science claims that have popped up in the past few weeks. So let’s stop all of this right here, right now: The Earth is round, not flat (and it’s definitely not hollow). Last year was the hottest year on record, and climate change is really happening (so please just stop, Mr. Cruz). And FFS, genetically modified mosquitoes didn’t start the Zika outbreak.