Chapter 16. None
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By PHYLLIS KORKKI Ever experienced a bout of anxiety at work? I just did. One day last week I had several assignments to finish in quick succession. I could feel thoughts pinging around in my brain as I tried and failed to decide what to focus on first. Once I was able to get the pandemonium under control, my brain felt like mush. So what did I do? I breathed deeply from the middle of my body. I imagined the top of my head, and pictured arrows coming out the sides of my shoulders. I stood up for a while and then walked around the newsroom. And went back to work. These simple solutions to anxiety are not so easy to practice in an era of multitasking, multiple screens and mindless distractions. I learned them only after signing a contract to write a book — and becoming so anxious about it that I developed back and stomach pains. Unable to score a prescription for Klonopin (it’s addictive, my doctor said), I was reduced to seeking out natural methods to relieve my anxiety. The methods I learned helped me write the book. But they also made me realize that workers of all stripes could use them to reduce stress, and to think more clearly and creatively. My first stop was Belisa Vranich, a clinical psychologist who teaches — or rather reteaches — people how to breathe. Dimly I sensed that the way I was inhaling and exhaling was out of whack, and she confirmed it by giving me some tests. First off, like most people, I was a “vertical” breather, meaning my shoulders moved upward when I inhaled. Second, I was breathing from my upper chest, where the lungs don’t have much presence. © 2016 The New York Times Company
Link ID: 22527 - Posted: 08.08.2016
Pete Etchells Mind gamers: How good do you reckon your memory is? We might forget things from time to time, but the stuff we do remember is pretty accurate, right? The trouble is, our memory isn’t as infallible as we might want to believe, and you can test this for yourself using the simple experiment below. All done? Great. Now we’re going to do a simple recognition test – below is another list of words for you to look at. Without looking back, note down which of them appeared in the three lists you just scanned. No cheating! If you said that top, seat and yawn were in the lists, you’re spot on. Likewise, if you think that slow, sweet and strong didn’t appear anywhere, you’re also right. What about chair, mountain and sleep though? They sound like they should have been in the lists, but they never made an appearance. Some of you may have spotted this, but a lot of people tend to say, with a fair amount of certainty, that the words were present. This experiment comes from a classic 1995 study by Henry L. Roediger and Kathleen McDermott at Rice University in Texas. Based on earlier work by James Deese (hence the name Deese-Roediger-McDermott, or DRM, paradigm), participants heard a series of word lists, which they then had to recall from memory. After a brief conversation with the researcher, the participants were then given a new list of words. Critically, this new list contained some words that were associated with every single item on each of the initial lists – for example, while sleep doesn’t appear on list 3 above, it’s related to each word that does appear (bed, rest, tired, and so on). © 2016 Guardian News and Media Limited
Keyword: Learning & Memory
Link ID: 22526 - Posted: 08.08.2016
By EUGENE M. CARUSO, ZACHARY C. BURNS and BENJAMIN A. CONVERSE Watching slow-motion footage of an event can certainly improve our judgment of what happened. But can it also impair judgment? This question arose in the 2009 murder trial of a man named John Lewis, who killed a police officer during an armed robbery of a Dunkin’ Donuts in Philadelphia. Mr. Lewis pleaded guilty; the only question for the jury was whether the murder resulted from a “willful, deliberate and premeditated” intent to kill or — as Mr. Lewis argued — from a spontaneous, panicked reaction to seeing the officer enter the store unexpectedly. The key piece of evidence was a surveillance video of the shooting, which the jury saw both in real time and in slow motion. The jury found that Mr. Lewis had acted with premeditation, and he was sentenced to death. Mr. Lewis appealed the decision, arguing that the slow-motion video was prejudicial. Specifically, he claimed that watching the video in slow motion artificially stretched the relevant time period and created a “false impression of premeditation.” Did it? We recently conducted a series of experiments whose results are strikingly consistent with that claim. Our studies, published this week in the Proceedings of the National Academy of Sciences, show that seeing replays of an action in slow motion leads viewers to believe that the actor had more time to think before acting than he actually did. The result is that slow motion makes actions seem more intentional, more premeditated. In one of our studies, participants watched surveillance video of a fatal shooting that occurred outside a convenience store during an armed robbery. We gave them a set of instructions similar to those given to the jurors in Mr. Lewis’s case, asking them to decide whether the crime was premeditated or not. We assigned half our participants to watch the video in slow motion and the other half to watch it at regular speed. © 2016 The New York Times Company
Link ID: 22525 - Posted: 08.08.2016
By MARTHA C. WHITE A graphic 30-year-old drug education campaign from Partnership for a Drug-Free America is being updated. For a generation of commercial-watching adolescents, it was an indelible image: an egg, sizzling in a frying pan, representing “your brain on drugs.” It was a straightforward message, and the ad’s final line — “Any questions?” — asked as the egg white clouded and cooked, was strictly rhetorical. Three decades later, the Partnership for Drug-Free Kids (the group formerly known as the Partnership for a Drug-Free America) is bringing the frying pan out of retirement and firing up the stove again. But this time questions are the point. The group hopes it can tap into the nostalgia parents may have for the old frying egg ad while also letting them know their children do indeed want answers about drugs. “‘Any questions’ was the end. Now it’s the beginning,” said Scott Seymour, chief creative officer at BFG Communications, which created print and digital banner ads for the new campaign. “The landscape of drugs has really gotten a lot more complex, so we took this idea of having a succession of questions delivered by kids,” he said. The group drew on real inquiries from parents to develop the questions featured in the ads, which cover topics like prescription drugs and marijuana legalization. Children today feel empowered and entitled to ask questions about drugs, and parents are more willing to entertain those questions, observers say. “Because of parenting styles today, parents are engaged with their kids in a different way,” said Kristi Rowe, chief marketing officer at the Partnership for Drug-Free Kids. “They’re really stumped by the questions. They don’t know how to answer them.” © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22524 - Posted: 08.08.2016
Helen Thompson A roughly 27-million-year-old fossilized skull echoes growing evidence that ancient whales could navigate using high-frequency sound. Discovered over a decade ago in a drainage ditch by an amateur fossil hunter on the South Carolina coast, the skull belongs to an early toothed whale. The fossil is so well-preserved that it includes rare inner ear bones similar to those found in modern whales and dolphins. Inspired by the Latin for “echo hunter,” scientists have now named the ancient whale Echovenator sandersi. “It suggests that the earliest toothed whales could hear high-frequency sounds,” which is essential for echolocation, says Morgan Churchill, an anatomist at the New York Institute of Technology in Old Westbury. Churchill and his colleagues describe the specimen online August 4 in Current Biology. Modern whales are divided on the sound spectrum. Toothed whales, such as orcas and porpoises, use high-frequency clicking sounds to sense predators and prey. Filter-feeding baleen whales, on the other hand, use low-frequency sound for long-distance communication. Around 35 million years ago, the two groups split, and E. sandersi emerged soon after. CT scans show that E. sandersi had a few features indicative of ultrasonic hearing in modern whales and dolphins. Most importantly, it had a spiraling inner ear bone with wide curves and a long bony support structure, both of which allow a greater sensitivity to higher-frequency sound. A small nerve canal probably transmitted sound signals to the brain. © Society for Science & the Public 2000 - 2016. All rights reserved.
By Roxanne Khamsi, What if controlling the appetite were as easy as flipping a switch? It sounds like the stuff of science fiction, but Jeffrey Friedman of Rockefeller University and his colleagues did exactly this in genetically engineered mice to try to shed light on how the brain influences appetite. Friedman and his colleagues used magnetic stimulation to switch on neurons in a region of the brain called the ventromedial hypothalamus and found that doing so increased the rodents' blood sugar levels and decreased levels of the hormone insulin. Turning on the neurons also caused the mice to eat more than their control counterparts. The ultimate confirmation came when they inhibited these neurons and saw the opposite effects: it drove blood sugar down, elevated insulin levels and suppressed the animals' urge to consume their chow. That the brain influences hunger is not an unexpected finding, but scientists have recently narrowed in on how it has sway on what ends up in the gut—and how the gut talks to the mind. This two-way communication, defined as the 'gut–brain axis', happens not only through nerve connections between the organs, but also through biochemical signals, such as hormones, that circulate in the body. “The idea that there is bidirectional communication between the gastrointestinal tract and brain that affects metabolism traces back more than a century,” Friedman says, referring to the work of the nineteenth-century French scientist Claude Bernard, who made seminal discoveries into how the body maintains physiological equilibrium. “Our new findings that insulin-producing cells in the pancreas can be controlled by certain neurons in the brain that sense blood sugar provides further experimental evidence supporting this notion.” © 2016 Scientific American,
Link ID: 22522 - Posted: 08.06.2016
By Nicholas Bakalar A drug used to treat rheumatoid arthritis may have benefits against Alzheimer’s disease, researchers report. Rheumatoid arthritis is an autoimmune disease believed to be driven in part by tumor necrosis factor, or T.N.F., a protein that promotes inflammation. Drugs that block T.N.F., including an injectable drug called etanercept, have been used to treat rheumatoid arthritis for many years. T.N.F. is also elevated in the cerebrospinal fluid of Alzheimer’s patients. Researchers identified 41,109 men and women with a diagnosis of rheumatoid arthritis and 325 with both rheumatoid arthritis and Alzheimer’s disease. In people over 65, the prevalence of Alzheimer’s disease was more than twice as high in people with rheumatoid arthritis as in those without it. The study is in CNS Drugs. But unlike patients treated with five other rheumatoid arthritis drugs, those who had been treated with etanercept showed a significantly reduced risk for Alzheimer’s disease. Still, the lead author, Dr. Richard C. Chou, an assistant professor of medicine at Dartmouth, said that it is too early to think of using etanercept as a treatment for Alzheimer’s. “We’ve identified a process in the brain, and if you can control this process with etanercept, you may be able to control Alzheimer’s,” he said. “But we need clinical trials to prove and confirm it.” © 2016 The New York Times Company
Link ID: 22520 - Posted: 08.06.2016
By LUKE DITTRICH ‘Can you tell me who the president of the United States is at the moment?” A man and a woman sat in an office in the Clinical Research Center at the Massachusetts Institute of Technology. It was 1986, and the man, Henry Molaison, was about to turn 60. He was wearing sweatpants and a checkered shirt and had thick glasses and thick hair. He pondered the question for a moment. “No,” he said. “I can’t.” The woman, Jenni Ogden, was a visiting postdoctoral research fellow from the University of Auckland, in New Zealand. One of the greatest thrills of her time at M.I.T. was the chance to have sit-down sessions with Henry. In her field — neuropsychology — he was a legendary figure, something between a rock star and a saint. “Who’s the last president you remember?” “I don’t. ... ” He paused for a second, mulling over the question. He had a soft, tentative voice, a warm New England accent. “Ike,” he said finally. Dwight D. Eisenhower’s inauguration took place in 1953. Our world had spun around the sun more than 30 times since, though Henry’s world had stayed still, frozen in orbit. This is because 1953 was the year he received an experimental operation, one that destroyed most of several deep-seated structures in his brain, including his hippocampus, his amygdala and his entorhinal cortex. The operation, performed on both sides of his brain and intended to treat Henry’s epilepsy, rendered him profoundly amnesiac, unable to hold on to the present moment for more than 30 seconds or so. That outcome, devastating to Henry, was a boon to science: By 1986, Patient H.M. — as he was called in countless journal articles and textbooks — had become arguably the most important human research subject of all time, revolutionizing our understanding of how memory works. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22519 - Posted: 08.04.2016
By Jonathan Webb Science reporter, BBC News Scientists have glimpsed activity deep in the mouse brain which can explain why we get thirsty when we eat, and why cold water is more thirst-quenching. A specific "thirst circuit" was rapidly activated by food and quietened by cooling down the animals' mouths. The same brain cells were already known to stimulate drinking, for example when dehydration concentrates the blood. But the new findings describe a much faster response, which predicts the body's future demand for water. The researchers went looking for this type of system because they were puzzled by the fact that drinking behaviour, in humans as well as animals, seems to be regulated very quickly. "There's this textbook model for homeostatic regulation of thirst, that's been around for almost 100 years, that's based on the blood," said the study's senior author Zachary Knight, from the University of California, San Francisco. "There are these neurons in the brain that… generate thirst when the blood becomes too salty or the blood volume falls too low. But lots of aspects of everyday drinking can't possibly be explained by that homeostatic model because they occur much too quickly." Take the "prandial thirst" that comes while we consume a big, salty meal - or the fact that we feel quenched almost as soon as we take a drink. © 2016 BBC.
Link ID: 22518 - Posted: 08.04.2016
By Alice Klein Rise and shine! Neuronal switches have been discovered that can suddenly rouse flies from slumber – or send them into a doze. There are several parallels between sleep in flies and mammals, making fruit flies a good choice for investigating how we sleep. One way to do this is to use optogenetics to activate specific neurons to see what they do. This works by using light to turn on cells genetically modified to respond to certain wavelengths. Gero Miesenböck at the University of Oxford and his team have discovered how to wake flies up. Using light as the trigger the team stimulated neurons that release a molecule called dopamine. The dopamine then switched off sleep-promoting neurons in what’s called the dorsal fan-shaped body, waking the flies. Meanwhile, Fang Guo at Brandeis University in Waltham, Massachusetts, and his team have found that activating neurons that form part of a fly’s internal clock will send it to sleep. When stimulated, these neurons released glutamate, which turned off activity-promoting neurons in the master pacemaker area of the brain. While human and fly brains are obviously very different in structure, being asleep or awake are similar states regardless of the kind of brain an animal has, says Bruno van Swinderen at the University of Queensland, Australia. © Copyright Reed Business Information Ltd.
By Sarah Kaplan Sleep just doesn't make sense. "Think about it," said Gero Miesenböck, a neuroscientist at the University of Oxford. "We do it. Every animal with a brain does it. But obviously it has considerable risks." Sleeping animals are incredibly vulnerable to attacks, with no obvious benefit to make up for it — at best, they waste precious hours that could be used finding food or seducing a mate; at worst, they could get eaten. "If evolution had managed to invent an animal that doesn’t need to sleep ... the selective advantage for it would be immense," Miesenböck said. "The fact that no such animal exists indicates that sleep is really vital, but we don't know why." But Miesenböck is part of team of sleep researchers who believe they are inching closer to to an answer. In a paper published in the journal Nature on Wednesday, they describe a cluster of two dozen brain cells in fruit flies that operate as a homeostatic sleep switch, turning on when the body needs rest and off again when it's time to wake up. "It's like a thermostat," Miesenböck said of the switch, "But instead of responding to temperature it responds to something else." If he and his colleagues could find out what that "something" is, "we might have the answer to the mystery of sleep."
By Anna Vlasits A small corner of the neuroscience world was in a frenzy. It was mid-June and a scientific paper had just been published claiming that years worth of results were riddled with errors. The study had dug into the software used to analyze one kind of brain scan, called functional MRI. The software’s approach was wrong, the researchers wrote, calling into doubt “the validity of some 40,000 fMRI studies”—in other words, all of them. The reaction was swift. Twitter lit up with panicked neuroscientists. Bloggers and reporters rained down headlines citing “seriously flawed” “glitches” and “bugs.” Other scientists thundered out essays defending their studies. Finally, one of the authors of the paper, published in Proceedings of the National Academy of Sciences, stepped into the fray. In a blog post, Thomas Nichols wrote, “There is one number I regret: 40,000.” Their finding, Nichols went on to write, only affects a portion of all fMRI papers—or, some scientists think, possibly none at all. It wasn’t nearly as bad as the hype suggested. The brief kerfuffle could just be dismissed as a tempest in a teapot, science’s self-correcting mechanisms in action. But the study, and its response, heralds a new level of self-scrutiny for fMRI studies, which have been plagued for decades by accusations of shoddy science and pop-culture pandering. fMRI, in other words, is growing up, but not without some pains along the way. A bumpy start for brain scanning © 2016 Scientific American,
Keyword: Brain imaging
Link ID: 22513 - Posted: 08.04.2016
The brains of overweight middle-aged people resemble brains that are a decade older in healthier people. A study of 473 adults has found that people who are overweight have less white matter, which connects different brain areas and enables signaling between them. The volume of white matter in the brains of overweight people at 50 were similar to that seen in the brains of lean people at 60. Human brains naturally shrink with age, but previous research has shown that this seems to happen more quickly in obese people. “As our brains age, they naturally shrink in size, but it isn’t clear why people who are overweight have a greater reduction in the amount of white matter,” says Lisa Ronan, at the University of Cambridge, a member of the research team. “We can only speculate on whether obesity might in some way cause these changes or whether obesity is a consequence of brain changes.” Intriguingly, the difference between lean and overweight people’s brains was only apparent from middle age onwards. It’s possible that this is because we are particularly vulnerable in some way at this time, says team-member Paul Fletcher, also at the University of Cambridge. However, despite this reduction in white matter, cognitive tests did not find any evidence that being overweight was linked to reduced brain function. “We don’t yet know the implications of these changes in brain structure,” says Sadaf Farooqi, at the University of Cambridge, who was also involved in the research. © Copyright Reed Business Information Ltd.
Link ID: 22512 - Posted: 08.04.2016
by Helen Thompson Pinky and The Brain's smarts might not be so far-fetched. Some mice are quicker on the uptake than others. While it might not lead to world domination, wits have their upside: a better shot at staying alive. Biologists Audrey Maille and Carsten Schradin of the University of Strasbourg in France tested reaction time and spatial memory in 90 African striped mice (Rhabdomys pumilio) over the course of a summer. For this particular wild rodent, surviving harsh summer droughts means making it to mating season in the early fall. The team saw some overall trends: Females were more likely to survive if they had quick reflexes, and males were more likely to survive if they had good spatial memory. Cognitive traits like reacting quickly and remembering the best places to hide are key to eluding predators during these tough times but may come with trade-offs for males and females. The results show that an individual mouse’s cognitive strengths are linked to its survival odds, suggesting that the pressure to survive can shape basic cognition, Maille and Schradin write August 3 in Biology Letters. |© Society for Science & the Public 2000 - 2016
By Alice Klein The debate has finally been put to bed. Wearable brainwave recorders confirm that birds do indeed sleep while flying, but only for brief periods and usually with one half of their brain. We know several bird species can travel vast distances non-stop, prompting speculation that they must nap mid-flight. Great frigatebirds, for example, can fly continuously for up to two months. On the other hand, the male sandpiper, for one, can largely forgo sleep during the breeding season, hinting that it may also be possible for birds to stay awake during prolonged trips. To settle this question, Niels Rattenborg at the Max Planck Institute for Ornithology in Seewiesen, Germany, and his colleagues fitted small brain activity monitors and movement trackers to 14 great frigatebirds. During long flights, the birds slept for an average of 41 minutes per day, in short episodes of about 12 seconds each. By contrast, they slept for more than 12 hours per day on land. Frigatebirds in flight tend to use one hemisphere at a time to sleep, as do ducks and dolphins, but sometimes they used both. “Some people thought that all their sleep would have to be unihemispheric otherwise they would drop from the sky,” says Rattenborg. “But that’s not the case – they can sleep with both hemispheres and they just continue soaring.” Sleep typically took place as the birds were circling in rising air currents, when they did not need to flap their wings. © Copyright Reed Business Information Ltd.
By Libby Copeland Don’t get him wrong: Dean Burnett loves the brain as much as the next neuroscientist. But if he’s being honest, it’s “really quite rubbish in a lot of ways,” he says. In his new book, Idiot Brain, Burnett aims to take our most prized organ down a peg or two. Burnett is most fascinated by the brain’s tendency to trip us up when it’s just trying to help. His book explores many of these quirks: How we edit our own memories to make ourselves look better without knowing it; how anger persuades us we can take on a bully twice our size; and what may cause us to feel like we’re falling and jerk awake just as we’re falling asleep. (It could have something to do with our ancestors sleeping in trees.) We caught up with Burnett, who is also a science blogger for The Guardian and a stand-up comic, to ask him some of our everyday questions and frustrations with neuroscience. Why is it that we get motion sickness when we’re traveling in a plane or a car? We haven’t evolved, obviously, to ride in vehicles; that’s a very new thing in evolutionary terms. So the main theory as to why we get motion sickness is that it’s essentially a conflict in the senses that are being relayed to the subcortical part of the brain where the senses are integrated together. The body and the muscles are saying we are still. Your eyes are saying the environment is still. The balance sense in the ears are detecting movement. The brain is getting conflicting messages from the fundamental senses, and in evolutionary terms there’s only one thing that can cause that, which is a neurotoxin. And as a result the brain thinks it’s been poisoned and what do you do when you’ve been poisoned? Throw up.
Link ID: 22508 - Posted: 08.03.2016
By Colby Itkowitz On any given day people face any number of minor annoyances such as being stuck in traffic or spilling coffee on their shirts or forgetting their keys. Then there’s the persistent stressors that come from work, relationships and finances. And there’s the uncontrollable anxieties of global terrorism, mass shootings and Zika-carrying mosquitoes. But why are some people able to deal with it all so calmly, while others freak out? A team of researchers at Yale University may have found the answer in the brain. The scientists studied the brains of 30 adult volunteers with no history of mental or physical health issues as they watched a slideshow of gruesome and terrifying images for six minutes. To compare brain activity, they then showed the participants benign images that would evoke little emotion, such as a photo of a chair. They located three areas of the brain that responded to the stress of seeing photos of people mutilated or at gunpoint or in other harrowing scenarios. But what the researchers found most interesting was how the ventromedial prefrontal cortex (vmPFC), which processes risk and emotional response, adapted while viewing the photos. In everyone, activity in that region decreased initially in response to the images, as though their guard was down, but then in some people, it became hyperactive, as if working overtime to control the emotional response, or in other words, to cope. “We have not had a way of breaking that apart to see what the brain is doing,” said Rajita Sinha, director of the Yale Stress Center and lead author of the study. “How do we cope in the moment? Here, we said, in the moment under acute threat how does the brain cope and regain control?” © 1996-2016 The Washington Post
Link ID: 22506 - Posted: 08.03.2016
By Katherine S. Pollard When the first human genome sequence was published in 2001,1 I was a graduate student working as the statistics expert on a team of scientists. Hailing from academia and biotechnology, we aimed to discover differences in gene expression levels between tumors and healthy cells. Like many others, I had high hopes for what we could do with this enormous text file of more than 3 billion As, Cs, Ts, and Gs. Ambitious visions of a precise wiring diagram for human cells and imminent cures for disease were commonplace among my classmates and professors. But I was most excited about a different use of the data, and I found myself counting the months until the genome of a chimpanzee would be sequenced. Chimps are our closest living relatives on the tree of life. While their biology is largely similar to ours, we have many striking differences, ranging from digestive enzymes to spoken language. Humans also suffer from an array of diseases that do not afflict chimpanzees or are less severe in them, including autism, schizophrenia, Alzheimer’s disease, diabetes, atherosclerosis, AIDS, rheumatoid arthritis, and certain cancers. I had long been fascinated with hominin fossils and the way the bones morphed into different forms over evolutionary time. But those skeletons cannot tell us much about the history of our immune system or our cognitive abilities. So I started brainstorming about how to extend the statistical approaches we were using for cancer research to compare human and chimpanzee DNA. My immodest goal was to identify the genetic basis for all the traits that make humans unique. © 1986-2016 The Scientist
By Bahar Gholipour After reflexively reaching out to grab a hot pan falling from the stove, you may be able to withdraw your hand at the very last moment to avoid getting burned. That is because the brain's executive control can step in to break a chain of automatic commands. Several new lines of evidence suggest that the same may be true when it comes to the reflex of recollection—and that the brain can halt the spontaneous retrieval of potentially painful memories. Within the brain, memories sit in a web of interconnected information. As a result, one memory can trigger another, making it bubble up to the surface without any conscious effort. “When you get a reminder, the mind's automatic response is to do you a favor by trying to deliver the thing that's associated with it,” says Michael Anderson, a neuroscientist at the University of Cambridge. “But sometimes we are reminded of things we would rather not think about.” Humans are not helpless against this process, however. Previous imaging studies suggest that the brain's frontal areas can dampen the activity of the hippocampus, a crucial structure for memory, and therefore suppress retrieval. In an effort to learn more, Anderson and his colleagues recently investigated what happens after the hippocampus is suppressed. They asked 381 college students to learn pairs of loosely related words. Later, the students were shown one word and asked to recall the other—or to do the opposite and to actively not think about the other word. Sometimes between these tasks they were shown unusual images, such as a peacock standing in a parking lot. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22500 - Posted: 08.01.2016
By NICHOLAS ST. FLEUR Orangutan hear, orangutan do. Researchers at the Indianapolis Zoo observed an orangutan mimic the pitch and tone of human sounds, for the first time. The finding, which was published Wednesday, provides insight into the evolutionary origin of human speech, the team said. “It really redefines for us what we know about the capabilities of orangutans,” said Rob Shumaker, director of the zoo and an author on the paper. “What we have to consider now is the possibility that the origins of spoken language are not exclusively human, and that they may have come from great apes.” Rocky, an 11-year-old orangutan at the zoo, has a special ability. He can make sounds using his vocal folds, or voice box, that resemble the vowel “A,” and sound like “Ah.” The noises, or “wookies” as the researchers called them, are variations of the same vocalization. Sometimes the great ape would say high-pitched “wookies” and sometimes he would say his “Ahs” in a lower pitch. The researchers note that the sounds are specific to Rocky and ones that he used everyday. No other orangutan, captive or wild, made these noises. Rocky, who had never lived in the rain forest, apparently learned the skill during his time as an entertainment orangutan before coming to the zoo. He was at one point the most seen orangutan in movies and commercials, according to the zoo. The researchers said that Rocky’s grunts show that great apes have the capacity to learn to control their muscles to deliberately alter their sounds in a “conversational” manner. The findings, which were published in the journal Scientific Reports, challenge the notion that orangutans — an endangered species that shares about 97 percent of it DNA with humans — make noises simply in response to something, sort of like how you might scream when you place your hand on a hot stove. © 2016 The New York Times Company