Chapter 16. None
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A study in Neurology suggests that analyzing levels of the protein p75ECD in urine samples from people with amyotrophic lateral sclerosis (ALS) may help monitor disease progression as well as determine the effectiveness of therapies. The study was supported by National Institute of Neurological Disorders and Stroke (NINDS) and National Center for Advancing Translational Sciences (NCATS), both part of the National Institutes of Health. Mary-Louise Rogers, Ph.D., senior research fellow at Flinders University in Adelaide, Australia, and Michael Benatar, M.D., Ph.D, professor of neurology at the University of Miami, and their teams, discovered that levels of urinary p75 ECD increased gradually in patients with ALS as their disease progressed over a 2-year study period. “It was encouraging to see changes in p75ECD over the course of the study, because it suggests an objective new method for tracking the progression of this aggressive disease,” said Amelie Gubitz, Ph.D., program director at NINDS. “In addition, it indicates the possibility of assessing whether levels of that protein decrease while patients try future treatments, to tell us whether the therapies are having any beneficial effects.” Further analysis of the samples from 54 patients revealed that those who began the study with lower levels of urinary p75ECD survived longer than did patients who had higher levels of the protein initially, suggesting that it could be a prognostic marker of the disease and may inform patients about their illness. Dr. Benatar and his team noted that this may be useful in selecting participants for clinical trials and in improving study design.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 23396 - Posted: 03.23.2017
By Jia Naqvi A drug frequently prescribed for pain is no more effective than a placebo at controlling sciatica, a common source of pain in the lower back and leg, according to a study published Wednesday in the New England Journal of Medicine. The researchers at the George Institute for Global Health in Australia followed 209 sciatica patients in Sydney who were randomly assigned to receive either the drug pregabalin, more commonly known as Lyrica, or a placebo. The results showed no significant differences in leg pain intensity between the group on the placebo and that on Lyrica after eight weeks taking the drug or during the rest of the year on follow-up exams. Similarly, there were no differences for other outcomes such as back pain, quality of life and degree of disability. After Lyrica was approved in 2004, it has become the most commonly prescribed medicine for neuropathic pain, which is caused by damage to the nervous system. The drug was ranked as the 19th-highest-earning pharmaceutical in 2015, with worldwide sales rising annually at a rate of 9 percent and sale revenue of more than $3 billion in 2015 in the United States. “We have seen a huge rise in the amount of prescriptions being written each year for patients suffering from sciatica. It’s an incredibly painful and disabling condition, so it’s no wonder people are desperate for relief and medicines such as pregabalin have been widely prescribed,” Christine Lin, one of the authors of the study and an associate professor at the George Institute for Global Health, said in a news release. © 1996-2017 The Washington Post
Keyword: Pain & Touch
Link ID: 23395 - Posted: 03.23.2017
By Sam Wong It takes brains to choose a good partner. In one of the first experiments to look at the cognitive demands of choosing a mate, female guppies with big brains showed a preference for more colourful males, while those with smaller brains showed no preference. In guppies, like most animals, females are choosy about who to mate with, since they invest more in their offspring than males, which don’t help care for them. They tend to prefer males with striking colour patterns and big tails, traits that have been linked to good foraging ability and health. By choosing a male with these qualities, female guppies give their offspring a good chance of inheriting the same useful traits. Despite this, females often go on to make different choices. Alberto Corral López and colleagues at Stockholm University wanted to find out if brain size could account for this. Corral López and his team tested 36 females bred to have large brains, 36 bred to have small brains, and 16 females similar to guppies found in the wild. Previous studies have shown that large-brained guppies perform better in cognitive tests, suggesting that they are smarter. Each female was given the opportunity to associate with two males, one more colourful than the other. Females are known to spend more time close to males they would prefer to mate with, so the team timed how long they spent with each male. © Copyright Reed Business Information Ltd
By Mo Costandi This map of London shows how many other streets are connected to each street, with blue representing simple streets with few connecting streets and red representing complex streets with many connecting streets. Credit: Joao Pinelo Silva The brain contains a built-in GPS that relies on memories of past navigation experiences to simulate future ones. But how does it represent new environments in order to determine how to navigate them successfully? And what happens in the brain when we enter a new space, or use satellite navigation (SatNav) technology to help us find our way around? Research published Tuesday in Nature Communications reveals two distinct brain regions that cooperate to simulate the topology of one’s environment and plan future paths through it when one is actively navigating. In addition, the research suggests both regions become inactive when people follow SatNav instructions instead of using their spatial memories. In a previous study researchers at University College London took participants on a guided tour through the streets of London’s Soho district and then used functional magnetic resonance imaging (fMRI) to scan their brains as they watched 10 different simulations of navigating those streets. Some of the movies required them to decide at intersections which way would be the shortest path to a predetermined destination; others came with instructions about which way to go at each junction. © 2017 Scientific American,
Keyword: Learning & Memory
Link ID: 23391 - Posted: 03.22.2017
Hannah Devlin Scientists have developed a new genetic test for Alzheimer’s risk that can be used to predict the age at which a person will develop the disease. A high score on the test, which is based on 31 genetic markers, can translate to being diagnosed many years earlier than those with a low-risk genetic profile, the study found. Those ranked in the top 10% in terms of risk were more than three times as likely to develop Alzheimer’s during the course of the study, and did so more than a decade before those who ranked in the lowest 10%. Strobe lighting provides a flicker of hope in the fight against Alzheimer’s Read more Rahul Desikan, of the University of California – who led the international effort, said the test could be used to calculate any individual’s risk of developing Alzheimer’s that year. “That is, if you don’t already have dementia, what is your yearly risk for AD onset, based on your age and genetic information,” he said. The so-called polygenic hazard score test was developed using genetic data from more than 70,000 individuals, including patients with Alzheimer’s disease and healthy elderly people. It is already known that genetics plays a powerful role in Alzheimer’s. Around a quarter of patients have a strong family history of the disease, and scientists have shown this is partly explained by a gene called ApoE, which comes in three versions, and is known to have a powerful influence on the risk of getting the most common late-onset type of Alzheimer’s. One version of ApoE appears to reduce risk by up to 40%, while those with two copies (one from each parent) of the high-risk version can increase risk by 12 times.
Link ID: 23390 - Posted: 03.22.2017
By KIM SEVERSON SONOMA, Calif. — The first thing Paula Wolfert wants to make a guest is coffee blended with butter from grass-fed cows and something called brain octane oil. She waves a greasy plastic bottle of the oil around her jumble of a kitchen like a preacher who has taken up a serpent. Never mind that this is the woman who introduced tagines, Aleppo pepper and cassoulet to American kitchens, wrote nine cookbooks and once possessed a palate the food writer Ruth Reichl declared the best she’d ever encountered. Ms. Wolfert, 78, has dementia. She can’t cook much, even if she wanted to. Which, by the way, she doesn’t. She learned she probably had Alzheimer’s disease in 2013, but she suspected something wasn’t right long before. Words on a page sometimes made no sense. Complex questions started to baffle her. Since she has always been an audacious and kinetic conversationalist with a touch of hypochondria, friends didn’t notice anything was wrong. Doctors spoke of “senior moments.” But she knew. One day, Ms. Wolfert went to make an omelet for her husband, the crime novelist William Bayer. She had to ask him how. The woman who once marched up to the French chef Jean-Louis Palladin and told him a dish didn’t have enough salt can no longer taste the difference between a walnut and a pecan, or smell whether the mushrooms are burning. The list of eight languages she once understood has been reduced to English. Maybe 40 percent of the words she knew have evaporated. “What am I going to do, cry about it?” Ms. Wolfert said in an interview at her home this month, the slap of her Brooklyn accent still sharp. After all, she points out, her first husband left her in Morocco with two small children and $2,000: “I cried for 20 minutes and I thought, ‘This isn’t going to do any good.’” © 2017 The New York Times Company
Link ID: 23389 - Posted: 03.22.2017
By NICHOLAS BAKALAR Some research has suggested that vitamin E and selenium supplements might lower the risk for Alzheimer’s disease, but a new long-term trial has found no evidence that they will. The study began as a randomized clinical trial in 2002 testing the supplements for the prevention of prostate cancer. When that study was stopped in 2009 because no effect was found, 3,786 of the original 7,540 men participated in a continuing study to test the antioxidants as a preventive for Alzheimer’s. The study, in JAMA Neurology, randomly assigned the men, whose average age was 67 at the start, to take either vitamin E, selenium, both supplements, or a placebo. By 2015, 4.4 percent of the men had dementia, but there was no difference between the groups. Neither selenium, vitamin E, nor both in combination were any more effective than a placebo. The study controlled for age, family history of Alzheimer’s disease, education, race, diabetes and other factors. The lead author, Richard J. Kryscio, a professor of statistics at the University of Kentucky, said that it is possible that different dosages or different types of selenium or vitamin E might show an effect. “We could have picked the wrong version or the wrong dose,” he said. “But there’s really no evidence that these supplements will make a difference down the road in preventing dementia.” © 2017 The New York Times Company
Link ID: 23388 - Posted: 03.22.2017
by Helen Thompson Aside from being adorable, sea otters and Indo-Pacific bottlenose dolphins share an ecological feat: Both species use tools. Otters crack open snails with rocks, and dolphins carry cone-shaped sponges to protect their snouts while scavenging for rock dwelling fish. Researchers have linked tool use in dolphins to a set of differences in mitochondrial DNA — which passes from mother to offspring — suggesting that tool-use behavior may be inherited. Biologist Katherine Ralls of the Smithsonian Institution in Washington, D.C., and her colleagues looked for a similar pattern in otters off the California coast. The team tracked diet (primarily abalone, crab, mussels, clams, urchins or snails) and tool use in the wild and analyzed DNA from 197 individual otters. Otters that ate lots of hard-shelled snails — and used tools most frequently — rarely shared a common pattern in mitochondrial DNA, nor were they more closely related to other tool-users than any other otter in the population. Unlike dolphins, sea otters may all be predisposed to using tools because their ancestors probably lived off mollusks, which required cracking open. However, modern otters only take up tools when their diet requires them, the researchers report March 21 in Biology Letters. |© Society for Science & the Public 2000 - 2017.
Link ID: 23386 - Posted: 03.22.2017
As the father of two sons with schizophrenia, author Ron Powers is familiar with the pain and frustration of dealing with a chronic, incurable disease of the brain. Powers' younger son, Kevin, was a talented musician whose struggles with schizophrenia began at age 17. Just before his 21st birthday, in 2005, Kevin took his own life. A few years later, Powers' older son, Dean, started experiencing symptoms of schizophrenia and had a psychotic break. "There is no greater ... feeling of helplessness than to watch two beloved sons deteriorate before [your] eyes, not knowing what to do to bring them back," Powers tells Fresh Air's Terry Gross. Powers' new book, No One Cares About Crazy People, is both a memoir about his sons and a history of how the mentally ill have been treated medically, legally and socially. Although Dean is now medicated and doing well, Powers notes that many people with schizophrenia don't receive the treatment they need — in part because they often don't believe they are ill. "This unwillingness to believe that one is afflicted has led to tremendous problems," Powers says. "To force that person into being helped is a violation of his or her civil rights ... and the law may penalize the care workers who give [people with schizophrenia] medications or admit them to a hospital against their will. ... That is the great reigning Catch-22 of the way our society deals — or fails to deal — with schizophrenia." © 2017 npr
Link ID: 23383 - Posted: 03.21.2017
By Chris Baraniuk It’s sometimes practically impossible to tell similar colours apart. Even side by side, they look the same. A special pair of spectacles gives us new power to see more distinct colours, and could one day help to spot counterfeit banknotes or counteract camouflage. The glasses, devised by a team at the University of Wisconsin-Madison, basically enhance the user’s colour vision, allowing them to see metamers – colours that look the same but give off different wavelengths of light – as recognisably distinct hues. Human colour vision relies on three types of cone cells that react to short (blue), medium (green) and long (red) wavelengths. While brushing up on his knowledge of the eye before teaching a photonics class, physicist Mikhail Kats had a brainwave. Could the eye be tricked into effectively having another type of cone cell? In theory, this could take our vision from being trichromatic, which uses three colour channels, to tetrachromatic. Some animals see in four (or more) channels. Goldfish, for example, have cells for red, blue, green and ultraviolet light. Some researchers suggest that a very small number of humans may be tetrachromats too. Read more: Human eye proteins detect red beyond red To make their glasses, Kats and his colleagues designed two colour filters, one for each eye that strip out specific parts of the blue light spectrum. With each eye receiving slightly different spectral information about blue things, the team hypothesised that any subtle differences in colour would be more pronounced. And they were right. © Copyright Reed Business Information Ltd
Link ID: 23381 - Posted: 03.21.2017
Cris Ledón-Rettig Picture a lion: The male has a luxuriant mane, the female doesn’t. This is a classic example of what biologists call sexual dimorphism – the two sexes of the same species exhibit differences in form or behavior. Male and female lions pretty much share the same genetic information, but look quite different. We’re used to thinking of genes as responsible for the traits an organism develops. But different forms of a trait – mane or no mane – can arise from practically identical genetic information. Further, traits are not all equally sexually dimorphic. While the tails of peacocks and peahens are extremely different, their feet, for example, are pretty much the same. Understanding how this variation of form – what geneticists call phenotypic variation – arises is crucial to answering several scientific questions, including how novel traits appear during evolution and how complex diseases emerge during a lifetime. So researchers have taken a closer look at the genome, looking for the genes responsible for differences between sexes and between traits within one sex. The key to these sexually dimorphic traits appears to be a kind of protein called a transcription factor, whose job it is to turn genes “on” and “off.” In our own work with dung beetles, my colleagues and I are untangling how these transcription factors actually lead to the different traits we see in males and females. A lot of it has to do with something called “alternative gene splicing” – a phenomenon that allows a single gene to encode for different proteins, depending on how the building blocks are joined together. © 2010–2017, The Conversation US, Inc.
Sara Reardon, Jeff Tollefson, Alexandra Witze & Erin Ross Funding for the National Oceanic and Atmospheric Administration’s weather satellites, which track hurricanes, would be maintained under the Trump plan. When it comes to science, there are few winners in US President Donald Trump’s first budget proposal. The plan, released on 16 March, calls for double-digit cuts for the Environmental Protection Agency (EPA) and the National Institutes of Health (NIH). It also lays the foundation for a broad shift in the United States’ research priorities, including a retreat from environmental and climate programmes. Rumours of the White House proposal have swirled for weeks, alarming many researchers who depend on government funding — and science advocates who worry that the Trump administration’s stance will jeopardize US leadership in fields ranging from climate science to cancer biology. It is not clear, however, how much of the plan will survive negotiations in Congress over the coming months. What could Trump’s budget for science mean for you? “Cutting [research and development] funding from our budget is the same as cutting the engines off an airplane that’s too heavy for take-off,” says Jason Rao, director of international affairs at the American Society for Microbiology in Washington DC. The greatest threats to the United States, he says, are those presented by infectious diseases, climate change and energy production — none of which can be addressed effectively without scientific research. © 2017 Macmillan Publishers Limited,
Link ID: 23376 - Posted: 03.20.2017
Obese people who get surgery to lose weight have half the risk of developing heart failure as do patients who make lifestyle changes to shed excess pounds, a recent study suggests. “We were surprised by the large difference in heart failure incidence between the two groups,” said lead study author Johan Sundstrom of Uppsala University in Sweden. It’s possible that gastric bypass patients had a lower risk of heart failure because they lost more weight than the group trying to do so without surgery. Researchers also found that losing 22 pounds by any means was tied to a 23 percent drop in heart failure risk. The study team examined data on 25,805 obese people who had gastric bypass surgery, which reduces the stomach to a small pouch, and 13,701 patients who were put on low-calorie diets. After following half of the patients for at least four years, people who had gastric bypass were found to be 46 percent less likely to have developed heart failure. After one year, surgery patients had an average weight loss 41.4 pounds greater than that of those who relied on diet and exercise, the study found. After two years, surgery was associated with an average weight loss that was 49.8 pounds more than those who undertook lifestyle changes. Some previous research has linked obesity to heart failure, and a growing body of evidence suggests that obesity might directly cause the heart condition, Sundstrom said. While the new study wasn’t designed to prove a causal relationship, it adds more evidence in support of this possibility. © 1996-2017 The Washington Post
Link ID: 23372 - Posted: 03.19.2017
By Anna Azvolinsky Delivering a CRISPR/Cas9–based therapy directly to the eye via a viral vector can prevent retinal degeneration in a mouse model of retinitis pigmentosa, a team led by researchers at the National Eye Institute reported in Nature Communications today (March 14). Retinitis pigmentosa, which affects around one in 4,000 people, causes retinal degeneration that eventually leads to blindness. The inherited disorder has been mapped to more than 60 genes (and more than 3,000 mutations), presenting a challenge for researchers working toward a gene therapy. The results of this latest study suggest that a broader, gene-editing–based therapeutic approach could be used to target many of the genetic defects underlying retinitis pigmentosa. “Given the lack of effective therapies for retinal degeneration, particularly the lack of therapies applicable to a broad range of different genetic varieties of this disease, this study represents a very exciting and important advance in our field,” Joseph Corbo, a neuropathologist at the Washington University School of Medicine in St. Louis who was not involved in the work, wrote in an email to The Scientist. This combination of “CRISPR technology with an adeno-associated virus vector, a system tried and true for delivering genetic information to the retina, may represent the first step in a global treatment approach for rod-mediated degenerative disease,” Shannon Boye, whose University of Florida lab develops gene replacement strategies for eye disorders, wrote in an email to The Scientist. © 1986-2017 The Scientist
Link ID: 23364 - Posted: 03.16.2017
By Mitch Leslie It sounds like a crazy way to improve your health—spend some time on a platform that vibrates at about the same frequency as the lowest string on a double bass. But recent research indicates that the procedure, known as whole-body vibration, may be helpful in illnesses from cerebral palsy to chronic obstructive pulmonary disease. Now, a new study of obese mice reveals that whole-body vibration provides similar metabolic benefits as walking on a treadmill, suggesting it may be useful for treating obesity and type II diabetes. “I think it’s very promising,” says exercise physiologist Lee Brown of the California State University in Fullerton, who wasn’t connected to the study. Although the effects are small, he says, researchers should follow-up to determine whether they can duplicate them in humans. Plenty of gyms feature whole-body vibration machines, and many athletes swear the activity improves their performance. The jiggling does seem to spur muscles to work harder, possibly triggering some of the same effects as exercise. But researchers still don’t know how the two compare, especially when it comes to people who are ill. So biomedical engineer Meghan McGee-Lawrence of the Medical College of Georgia in Augusta and colleagues decided to perform a head-to-head comparison of exercise and whole-body vibration. The researchers tested mutant mice resistant to the appetite-controlling hormone leptin, resulting in obesity and diabetes. © 2017 American Association for the Advancement of Science.
Link ID: 23362 - Posted: 03.16.2017
By Christof Koch We moderns take it for granted that consciousness is intimately tied up with the brain. But this assumption did not always hold. For much of recorded history, the heart was considered the seat of reason, emotion, valor and mind. Indeed, the first step in mummification in ancient Egypt was to scoop out the brain through the nostrils and discard it, whereas the heart, the liver and other internal organs were carefully extracted and preserved. The pharaoh would then have access to everything he needed in his afterlife. Everything except for his brain! Several millennia later Aristotle, one of the greatest of all biologists, taxonomists, embryologists and the first evolutionist, had this to say: “And of course, the brain is not responsible for any of the sensations at all. The correct view [is] that the seat and source of sensation is the region of the heart.” He argued consistently that the primary function of the wet and cold brain is to cool the warm blood coming from the heart. Another set of historical texts is no more insightful on this question. The Old and the New Testaments are filled with references to the heart but entirely devoid of any mentions of the brain. Debate about what the brain does grew ever more intense over ensuing millennia. The modern embodiment of these arguments seeks to identify the precise areas within the three-pound cranial mass where consciousness arises. What follows is an attempt to size up the past and present of this transmillennial journey. The field has scored successes in delineating a brain region that keeps the neural engine humming. Switched on, you are awake and conscious. In another setting, your body is asleep, yet you still have experiences—you dream. In a third position, you are deeply asleep, effectively off-line. © 2017 Scientific American
Link ID: 23361 - Posted: 03.16.2017
Ian Sample Science editor Researchers have overcome one of the major stumbling blocks in artificial intelligence with a program that can learn one task after another using skills it acquires on the way. Developed by Google’s AI company, DeepMind, the program has taken on a range of different tasks and performed almost as well as a human. Crucially, and uniquely, the AI does not forget how it solved past problems, and uses the knowledge to tackle new ones. The AI is not capable of the general intelligence that humans draw on when they are faced with new challenges; its use of past lessons is more limited. But the work shows a way around a problem that had to be solved if researchers are ever to build so-called artificial general intelligence (AGI) machines that match human intelligence. “If we’re going to have computer programs that are more intelligent and more useful, then they will have to have this ability to learn sequentially,” said James Kirkpatrick at DeepMind. The ability to remember old skills and apply them to new tasks comes naturally to humans. A regular rollerblader might find ice skating a breeze because one skill helps the other. But recreating this ability in computers has proved a huge challenge for AI researchers. AI programs are typically one trick ponies that excel at one task, and one task only.
By MATT RICHTEL Amid an opioid epidemic, the rise of deadly synthetic drugs and the widening legalization of marijuana, a curious bright spot has emerged in the youth drug culture: American teenagers are growing less likely to try or regularly use drugs, including alcohol. With minor fits and starts, the trend has been building for a decade, with no clear understanding as to why. Some experts theorize that falling cigarette-smoking rates are cutting into a key gateway to drugs, or that antidrug education campaigns, long a largely failed enterprise, have finally taken hold. But researchers are starting to ponder an intriguing question: Are teenagers using drugs less in part because they are constantly stimulated and entertained by their computers and phones? The possibility is worth exploring, they say, because use of smartphones and tablets has exploded over the same period that drug use has declined. This correlation does not mean that one phenomenon is causing the other, but scientists say interactive media appears to play to similar impulses as drug experimentation, including sensation-seeking and the desire for independence. Or it might be that gadgets simply absorb a lot of time that could be used for other pursuits, including partying. Nora Volkow, director of the National Institute on Drug Abuse, says she plans to begin research on the topic in the next few months, and will convene a group of scholars in April to discuss it. The possibility that smartphones were contributing to a decline in drug use by teenagers, Dr. Volkow said, was the first question she asked when she saw the agency’s most recent survey results. The survey, “Monitoring the Future,” an annual government-funded report measuring drug use by teenagers, found that past-year use of illicit drugs other than marijuana was at the lowest level in the 40-year history of the project for eighth, 10th and 12th graders. © 2017 The New York Times Company
Keyword: Drug Abuse
Link ID: 23357 - Posted: 03.15.2017
Heidi Ledford Like a zombie that keeps on kicking, legal battles over mutant mice used for Alzheimer’s research are haunting the field once again — four years after the last round of lawsuits. In the latest case, the University of South Florida (USF) in Tampa has sued the US National Institutes of Health (NIH) for authorizing the distribution of a particular type of mouse used in the field. The first pre-trial hearing in the case is set to begin in a federal court on 21 March. The university holds a patent on the mouse, but the NIH has contracted the Jackson Laboratory, a non-profit organization in Bar Harbor, Maine, to supply the animals to researchers. The USF is now claiming that it deserves some of the money that went to the contractor. If the suit, filed in December 2015, is successful, it could set a precedent for other universities, cautions Robert Cook-Deegan, an intellectual-property scholar at the Washington DC centre of Arizona State University in Tempe. And that would threaten the affordability of and access to lab animals used to investigate. “It feels greedy to me,” Cook-Deegan says. “If other universities start doing this, all it does is push up the cost of research tools.” The mice, on which the USF filed a patent in 1997, express mutated forms of two genes1. These modifications help researchers to study how amyloid plaques develop in the brain, and enable them to investigate behavioural changes that manifest before those plaques appear. © 2017 Macmillan Publishers Limited,
Link ID: 23356 - Posted: 03.15.2017
Jon Hamilton An orangutan named Rocky is helping scientists figure out when early humans might have uttered the first word. Rocky, who is 12 and lives at the Indianapolis Zoo, has shown that he can control his vocal cords much the way people do. He can learn new vocal sounds and even match the pitch of sounds made by a person. "Rocky, and probably other great apes, can do things with their vocal apparatus that, for decades, people have asserted was impossible," says Rob Shumaker, the zoo's director, who has studied orangutans for more than 30 years. Rocky's abilities suggest that our human ancestors could have begun speaking 10 million years ago, about the time humans and great apes diverged, Shumaker says. Until now, many scientists thought that speech required changes in the brain and vocal apparatus that evolved more recently, during the past 2 million years. The vocal abilities of orangutans might have gone undetected had it not been for Rocky, an ape with an unusual past and a rare relationship with people. Rocky was separated from his mother soon after he was born, and spent his early years raised largely by people, and working in show business. "He was certainly the most visible orangutan in entertainment at the time," says Shumaker. "TV commercials, things like that."