Chapter 16. None
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By Elizabeth Pennisi Last week, researchers expanded the size of the mouse brain by giving rodents a piece of human DNA. Now another team has topped that feat, pinpointing a human gene that not only grows the mouse brain but also gives it the distinctive folds found in primate brains. The work suggests that scientists are finally beginning to unravel some of the evolutionary steps that boosted the cognitive powers of our species. “This study represents a major milestone in our understanding of the developmental emergence of human uniqueness,” says Victor Borrell Franco, a neurobiologist at the Institute of Neurosciences in Alicante, Spain, who was not involved with the work. The new study began when Wieland Huttner, a developmental neurobiologist at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany, and his colleagues started closely examining aborted human fetal tissue and embryonic mice. “We specifically wanted to figure out which genes are active during the development of the cortex, the part of the brain that is greatly expanded in humans and other primates compared to rodents,” says Marta Florio, the Huttner graduate student who carried out the main part of the work. That was harder than it sounded. Building a cortex requires several kinds of starting cells, or stem cells. The stem cells divide and sometimes specialize into other types of “intermediate” stem cells that in turn divide and form the neurons that make up brain tissue. To learn what genes are active in the two species, the team first had to develop a way to separate out the various types of cortical stem cells. © 2015 American Association for the Advancement of Science
by Helen Thomson We meet in a pub, we have a few drinks, some dinner and then you lean in for a kiss. You predict, based on our previous interactions, that the kiss will be reciprocated – rather than landing you with a slap in the face. All our social interactions require us to anticipate another person's undecided intentions and actions. Now, researchers have discovered specific brain cells that allow monkeys to do this. It is likely that the cells do the same job in humans. Keren Haroush and Ziv Williams at Harvard Medical School trained monkeys to play a version of the prisoner's dilemma, a game used to study cooperation. The monkeys sat next to each other and decided whether or not they wanted to cooperate with their companion, by moving a joystick to pick either option. Moving the joystick towards an orange circle meant cooperate, a blue triangle meant "not this time". Neither monkey could see the other's face, or receive any clues about their planned action. If the monkeys cooperated, both received four drops of juice. If one cooperated and the other decided not to, the one who cooperated received one drop, and the other received six drops of juice. If both declined to work together they both received two drops of juice. Once both had made their selections, they could see what the other monkey had chosen and hear the amount of juice their companion was enjoying. © Copyright Reed Business Information Ltd.
Link ID: 20627 - Posted: 02.27.2015
By Michael Erard Freckle, a male rhesus monkey, was greeted warmly by his fellow monkeys at his new home in Amherst, Massachusetts, when he arrived in 2000. But he didn’t return the favor: He terrorized his cagemate by stealing his fleece blanket and nabbed each new blanket the researchers added, until he had 10 and his cagemate none. After a few months, Freckle had also acquired a new name: Ivan, short for Ivan the Terrible. Freckle/Ivan, now at Melinda Novak’s primate research lab at the University of Massachusetts, may be unusual in having two names, but all of his neighbors have at least one moniker, Novak says. “You can say, ‘Kayla and Zoe are acting out today,’ and everybody knows who Kayla and Zoe are,” Novak says. “If you say ‘ZA-56 and ZA-65 are acting up today,’ people pause.” Scientists once shied away from naming research animals, and many of the millions of mice and rats used in U.S. research today go nameless, except for special individuals. But a look at many facilities suggests that most of the other 891,161 U.S. research animals have proper names, including nonhuman primates, dogs, pigs, rabbits, cats, and sheep. Rats are Pia, Splinter, Oprah, Persimmon. Monkeys are Nyah, Nadira, Tas, Doyle. One octopus is called Nixon. Breeder pairs of mice are “Tom and Katie,” or “Brad and Angelina.” If you’re a mouse with a penchant for escape, you’ll be Mighty Mouse or Houdini. If you’re a nasty mouse, you’ll be Lucifer or Lucifina. Animals in research are named after shampoos, candy bars, whiskeys, family members, movie stars, and superheroes. They’re named after Russians (Boris, Vladimir, Sergei), colors, the Simpsons, historical figures, and even rival scientists. These unofficial names rarely appear in publications, except sometimes in field studies of primates. But they’re used daily. © 2015 American Association for the Advancement of Science.
Keyword: Animal Rights
Link ID: 20625 - Posted: 02.27.2015
People with attention deficit hyperactivity disorder are about twice as likely to die prematurely as those without the disorder, say researchers. Researchers followed 1.92 million Danes, including 32,000 with ADHD, from birth through to 2013. "In this nationwide prospective cohort study with up to 32-year followup, children, adolescents and adults with ADHD had decreased life expectancy and more than double the risk of death compared with people without ADHD," Soren Dalsgaard, from Aarhus University in Denmark, and his co-authors concluded in Wednesday's online issue of Lancet. Actress Kirstie Alley holds a picture of Raymond Perone while testifying in favour of a bill designed to curb the over-prescribing of psychotropic drugs. Danish researchers studying ADHD say medications can reduce symptoms of inattention and impulsivity. (Phil Coale/Associated Press) "People diagnosed with ADHD in adulthood had a greater risk of death than did those diagnosed in childhood and adolescence. This finding could be caused by persistent ADHD being a more severe form of the disorder." Of the 107 individuals with ADHD who died, information on cause of death was available for 79. Of those, 25 died from natural causes and 54 from unnatural causes, including 42 from accidents. Being diagnosed with ADHD along with oppositional defiant disorder, conduct disorder and substance use disorder also increased the risk of death, the researchers found. Mortality risk was also higher for females than males, which led Dalsgaard to stress the need for early diagnosis, especially in girls and women, and to treat co-existing disorders. Although talk of premature death will worry parents and patients, they can seek solace in knowing the absolute risk of premature death at an individual level is low and can be greatly reduced with treatment, Stephen Faraone, a professor of psychiatry and director of child and adolescent psychiatry research at SUNY Upstate Medical University in New York, said in a journal commentary published with the study. ©2015 CBC/Radio-Canada.
Julie Beck When Paul Ekman was a grad student in the 1950s, psychologists were mostly ignoring emotions. Most psychology research at the time was focused on behaviorism—classical conditioning and the like. Silvan Tomkins was the one other person Ekman knew of who was studying emotions, and he’d done a little work on facial expressions that Ekman saw as extremely promising. “To me it was obvious,” Ekman says. “There’s gold in those hills; I have to find a way to mine it.” For his first cross-cultural studies in the 1960s, he traveled around the U.S., Chile, Argentina, and Brazil. In each location, he showed people photos of different facial expressions and asked them to match the images with six different emotions: happiness, sadness, anger, surprise, fear, and disgust. “There was very high agreement,” Ekman says. People tended to match smiling faces with “happiness,” furrow-browed, tight-lipped faces with “anger,” and so on. But these responses could have been influenced by culture. The best way to test whether emotions were truly universal, he thought, would be to repeat his experiment in a totally remote society that hadn’t been exposed to Western media. So he planned a trip to Papua New Guinea, his confidence bolstered by films he’d seen of the island’s isolated cultures: “I never saw an expression I wasn’t familiar with in our culture,” he says. Once there, he showed locals the same photos he’d shown his other research subjects. He gave them a choice between three photos and asked them to pick images that matched various stories (such as “this man’s child has just died”). Adult participants chose the expected emotion between 28 and 100 percent of the time, depending which photos they were choosing among. (The 28 percent was a bit of an outlier: That was when people had to choose between fear, surprise, and sadness. The next lowest rate was 48 percent.) © 2014 by The Atlantic Monthly Group.
Link ID: 20619 - Posted: 02.26.2015
by Hal Hodson Video: Bionic arm trumps flesh after elective amputation Bionic hands are go. Three men with serious nerve damage had their hands amputated and replaced by prosthetic ones that they can control with their minds. The procedure, dubbed "bionic reconstruction", was carried out by Oskar Aszmann at the Medical University of Vienna, Austria. The men had all suffered accidents which damaged the brachial plexus – the bundle of nerve fibres that runs from the spine to the hand. Despite attempted repairs to those nerves, the arm and hand remained paralysed. "But still there are some nerve fibres present," says Aszmann. "The injury is so massive that there are only a few. This is just not enough to make the hand alive. They will never drive a hand, but they might drive a prosthetic hand." This approach works because the prosthetic hands come with their own power source. Aszmann's patients plug their hands in to charge every night. Relying on electricity from the grid to power the hand means all the muscles and nerves need do is send the right signals to a prosthetic. Before the operation, Aszmann's patients had to prepare their bodies and brains. First he transplanted leg muscle into their arms to boost the signal from the remaining nerve fibres. Three months later, after the nerves had grown into the new muscle, the men started training their brains. © Copyright Reed Business Information Ltd.
Link ID: 20617 - Posted: 02.26.2015
By Jocelyn Kaiser The number of animals used by the top federally funded U.S. biomedical research institutions has risen 73% over 15 years, a “dramatic increase” driven mostly by more mice, concludes an animal rights group. They say researchers are not doing enough to reduce their use of mice, which are exempt from some federal animal protection laws. The National Institutes of Health (NIH), which collected the data, says the analysis by People for the Ethical Treatment of Animals (PETA) is “inappropriate.” The analysis was published online today in the Journal of Medical Ethics. Although the Animal Welfare Act requires that the U.S. Department of Agriculture track research labs’ use of cats, dogs, and nonhuman primates, smaller vertebrates—including mice, rats, fish, and birds bred for research—are exempt. To get a sense of the trends, PETA filed Freedom of Information Act requests for data from inventories that NIH-funded institutions must submit to NIH every 4 years to receive an “assurance” allowing them to do animal research. Looking at the 25 top NIH-funded institutions, PETA found these institutions housed a daily average of about 74,600 animals between 1997 and 2003; that leaped to an average of about 128,900 a day by 2008 to 2012, a 73% increase. (Because institutions don’t report at the same time, PETA combined figures over three time periods.) © 2015 American Association for the Advancement of Science
Keyword: Animal Rights
Link ID: 20616 - Posted: 02.26.2015
By KATIE THOMAS The retired tennis player Monica Seles spent this month making the rounds of television talk shows, appearing on everything from “Good Morning America” to “The Dr. Oz Show” to share her personal struggle with binge eating. “It took a while until I felt comfortable talking about it,” she said in a People magazine interview, explaining that she secretly devoured food for years while she was a professional athlete. “That’s one of the reasons I decided to do this campaign: to raise awareness that binge eating is a real medical condition.” But that is not the only reason. Ms. Seles is a paid spokeswoman for Shire, which late last month won approval to market its top-selling drug, Vyvanse, to treat binge-eating disorder, a condition that once existed in the shadow of better-known disorders like anorexia and bulimia but was officially recognized as its own disorder in 2013 by the American Psychiatric Association. As Shire introduces an ambitious campaign to promote Vyvanse but also to raise awareness about the disorder, some are saying the company is going too far to market a drug, a type of amphetamine, that is classified by the federal government as having a high potential for abuse. Shire’s track record is adding to the worry: The company helped put another once-stigmatized condition — attention deficit hyperactivity disorder — on the medical map and made billions of dollars from the sale of drugs, like Vyvanse and Adderall, to treat it. In recent years, federal officials have cited the company for inappropriately marketing Vyvanse and other A.D.H.D. drugs. In addition, some drug safety experts questioned why the Food and Drug Administration so swiftly approved the drug for binge eating — seeking little outside input — despite the fact that, for decades, amphetamines, which suppress the appetite, were widely abused as a treatment for obesity. © 2015 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 20614 - Posted: 02.25.2015
Helen Shen Repeated head injuries in American football have been linked to a degenerative brain disorder later in life. Dave Duerson suspected that something was wrong with his brain. By 2011, 18 years after the former American football player had retired from the Phoenix Cardinals, he experienced frequent headaches, memory problems and an increasingly short temper. Before he killed himself, he asked that his brain be donated for study. Researchers who examined it found signs of chronic traumatic encephalopathy (CTE), a degenerative condition linked to repeated head injuries. At least 69 cases have been reported in the literature since 2000, many in former boxers and American football players (P. H. Montenigro et al. Alz. Res. Ther. 6, 68; 2014) — heightening public concern about concussions during contact sports. Yet much about CTE is unknown, from its frequency to its precise risk factors and even whether its pathology is unique. Researchers now hope to take a major step towards answering those questions. At Boston University in Massachusetts on 25–27 February, neuroscientists will convene to examine the characteristics of CTE in brain tissue from post-mortem examinations. They hope to agree on a set of diagnostic criteria for the disease, and to assess whether it is distinct from other brain disorders, such as Alzheimer’s disease. The effort is sorely needed, says Walter Koroshetz, acting director of the US National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, which is organizing the meeting. “The definition is the important piece that lets you do the rest of the research,” he says. And the stakes are high. CTE is associated with memory loss, irritability, depression and explosive anger, which are thought to appear and worsen years after repeated head trauma. © 2015 Nature Publishing Group
Keyword: Brain Injury/Concussion
Link ID: 20613 - Posted: 02.25.2015
By Sandhya Sekar It’s stressful being a low-ranking hyena—so stressful that even their chromosomes feel it. Researchers have discovered that the challenges of African savanna hyena society shorten underdogs’ telomeres, stretches of DNA that bookend chromosomes and protect them from wear and tear during cell replication. The stress may come from the top hyenas getting the best meat, whereas lower ranking individuals have to travel long distances—sometimes to the edges of the group territory—to fend for themselves. With increased stress, higher amounts of stress hormones and cellular byproducts like oxygen ions and peroxides are produced, both of which have been shown to shorten telomeres in other species. When telomeres fall below a certain length, cells go into damage-control mode and kick off biochemical pathways that can result in cell death. The study, the team reports online today in Biology Letters, is the first to show that the stress of social hierarchy can shorten telomeres in a wild species. © 2015 American Association for the Advancement of Science.
Link ID: 20611 - Posted: 02.25.2015
by Penny Sarchet An injection and a dash of exercise could be the secret to keeping trim. These rainbow mice, imaged in infrared to reveal how much energy they are burning while on a treadmill, are revealing how a shot can boost a muscle's ability to burn calories. Red body parts show where lots of energy is being used. The mouse on the right has a red patch on its left hind leg, which corresponds to the spot where it received an injection of a substance developed by Denice Hodgson-Zingman from the University of Iowa and colleagues. The substance is a type of morpholino, a compound that can be designed to target specific genes, in this case to alter proteins responsible for storing energy. The disruption causes muscles to burn more energy even during mild exercise, such as a gentle trot on a treadmill. In contrast, the untreated mouse on the left, which is doing the same amount of exercise, is using less energy in the same spot, as illustrated by the colder green colour. The researchers hope the injection will help people who want to burn more calories do so through routine everyday activities, eliminating the need for intense exercise. Journal reference: Molecular Therapy, DOI: 10.1038/mt.2015.2141 © Copyright Reed Business Information Ltd.
Link ID: 20610 - Posted: 02.24.2015
By Aleksandra Sagan, CBC News Photos of emaciated women proudly displaying their protruding hips and ribs, as well as thinspirational quotes "fat-shaming" those who dare to eat, continue to thrive on social media, despite the best attempts by sites like Instagram to temper the reach of the pro-eating disorder community. Some girls gain thousands of followers posting pictures of "thigh gaps" and "bikini bridges," as well as underweight celebrities and thinspirational quotes like model Kate Moss's mantra: "nothing tastes as good as skinny feels." "It just provides a lot of positivity for them, just in a very maladaptive way," says Edward Selby, of the more visual outlet that sites like Instagram provide. An assistant professor of clinical psychology at Rutgers University in New Jersey, Selby is the director of a lab there that studies what makes people more likely to develop anorexia (self-starvation), bulimia (binge-eating and purging) and other eating disorders. About one in 20 young women in Canada has an eating disorder, according to the Toronto-based National Initiative for Eating Disorders. And people suffering from these diseases often feel good after exercising, purging, swallowing a laxative or doing other things that contribute to their illness, Selby says. They get caught in a "cyclic feedback loop," with the positive emotions pushing them to engage more in these risky behaviours. Online pro-anorexia and bulimia communities simply add to that loop by celebrating a person's unhealthy achievements, he says. "Finally under 130! Woohoo!" writes one user with a photo of her feet on a scale. "Yay congrats," reads a response. Another girl posts a screen grab from an app claiming that she's been fasting for more than a day. It receives 32 likes and a "great job" among the comments. ©2015 CBC/Radio-Canada
Keyword: Anorexia & Bulimia
Link ID: 20607 - Posted: 02.24.2015
By JON PALFREMAN EUGENE, Ore. — FOUR years ago, I was told I had Parkinson’s disease, a condition that affects about one million Americans. The disease is relentlessly progressive; often starting with a tremor in one limb on one side of the body, it spreads. The patient’s muscles become more rigid, frequently leading to a stooped posture, and movements slow down and get smaller and less fluid. As the disease advances — usually over a number of years — the patient becomes more and more disabled, experiencing symptoms from constipation to sleep disorders to cognitive impairment. Can Parkinson’s be slowed, stopped or even reversed? Can the disease be prevented before it starts, like polio and smallpox? More than at any time in history, success seems possible. Having sequenced the human genome, biomedical researchers have now set their sights on the ultimate frontier — the human brain. The formidable puzzle is to figure out how a three-pound lump of mostly fatty matter enables us to perform a seemingly endless number of tasks, like walking, seeing, hearing, smelling, tasting, touching, thinking, loving, hating, speaking and writing ... and why those awesome abilities break down with neurological disease. Many scientists view Parkinson’s as a so-called pathfinder. If they can figure out what causes Parkinson’s, it may open the door to understanding a host of other neurodegenerative diseases — and to making sense of an organ of incredible complexity. In Parkinson’s, the circuitry in a tiny region of the brain called the basal ganglia becomes dysfunctional. Along with the cerebellum, the basal ganglia normally acts as a kind of adviser that helps people learn adaptive skills by classic conditioning — rewarding good results with dopamine bursts and punishing errors by withholding the chemical. Babies rely on the basal ganglia to learn how to deploy their muscles to reach, grab, babble and crawl, and later to accomplish many complex tasks without thinking. For example, when a tennis player practices a stroke over and over again, the basal ganglia circuitry both rewards and “learns” the correct sequence of activities to produce, say, a good backhand drive automatically. © 2015 The New York Times Company
Link ID: 20606 - Posted: 02.24.2015
By Sandra G. Boodman Catherine Cutter’s voice was her livelihood. A professor of food science at Penn State University, the microbiologist routinely lectured to large classes about food safety in the meat and poultry industries. But in 2008, after Cutter’s strong alto voice deteriorated into a raspy whisper, she feared her academic career might be over.How could she teach if her students could barely hear her? The classroom wasn’t the only area of Cutter’s life affected by her voicelessness. The mother of two teenagers, Cutter, now 52, recalls that she “couldn’t yell — or even talk” to her kids and would have to knock on a wall or countertop to get their attention. Social situations became increasingly difficult as well, and going to a restaurant was a chore. Using the drive-through at her bank or dry cleaner was out of the question because she couldn’t be heard. “I just retreated,” said Cutter, who sought assistance from nearly two dozen specialists for her baffling condition. The remedies doctors prescribed — when they worked at all — resulted in improvement that was temporary at best. For two years Cutter searched in vain for help. It arrived in the form of a neurosurgeon she consulted for a second opinion about potentially risky surgery to correct a different condition. He suggested a disorder that had never been mentioned, a diagnosis that proved to be correct — and correctable. Until then, “everyone had been looking in the wrong place,” Cutter said.
Keyword: Movement Disorders
Link ID: 20605 - Posted: 02.24.2015
A dozen university students have been treated at Connecticut hospitals after overdosing on "Molly" or MDMA, a popular synthetic party drug. Police are investigating after the overdoses were reported late Sunday on the campus of Wesleyan University in Middletown, Connecticut. By Monday, eight remained in hospital and two were in critical condition. It was unclear whether the students had been together or where the drugs had come from. Middletown Police Chief William McKenna said that their "first and foremost goal is to obtain information on the batch of Molly that was distributed to the students on the campus," adding, "this information is critical in ensuring the recovery of those students affected." A pure and more powerful form of MDMA often sold as "Molly" can cause liver, kidney, cardiovascular failure, or death. In a campus-wide statement, Wesleyan president Michael S Roth urged students to "please, please stay away from illegal substances, the use of which can put you in extreme danger. One mistake can change your life forever". Dean Michael Whaley, vice president of student affairs at Wesleyan University, sent a letter to the school body on Sunday recommending students to check on their friends. Ten of the 12 people were Wesleyan students. In 2013, Molly-related deaths and illnesses forced the Electric Zoo Festival in New York to shut down early after two young people died and four were confined to hospital.
Keyword: Drug Abuse
Link ID: 20602 - Posted: 02.24.2015
|By Roni Jacobson Several pharmaceutical drugs promise to help addicts quit, and many people embrace the ease of popping a pill. Yet research continues to show that although medication can help, support networks and therapy targeting the underlying behaviors are still the best available ways to kick addiction over the long term. In addition, some of these medications come with scary side effects—hundreds of people have reportedly committed suicide while on the smoking-cessation drug Chantix, for example. Read on for short profiles of the addiction drugs currently on the market, as well as a few compounds that may hit shelves soon. © 2015 Scientific American,
Keyword: Drug Abuse
Link ID: 20601 - Posted: 02.24.2015
By ABIGAIL ZUGER, M.D. On an early summer night in 1944, on the wooded shoulder of a rural Massachusetts highway, a man in a rumpled brown suit wandered in the shadows. Whenever a car passed, he dropped to the ground and lay flat. His hair was matted, his face smeared with mud. He was a respectable Boston doctor on the lam, hungry, lost and ill. He was Mimi Baird’s father, Dr. Perry Baird, a Texas-born, Harvard-trained physician whose severe bipolar disease ultimately destroyed his life and scarred his family with the usual wide-ranging cruelties of mental illness. Dr. Baird vanished from Ms. Baird’s life when she was a little girl. She saw him once, briefly, when she was a teenager, then never again. He died in his mid-50s, in 1959. More than 30 years later, when Ms. Baird herself was in her 50s, a large package arrived on her doorstep and her father re-entered her world. The box contained a manuscript long forgotten in a relative’s garage, written in smudged pencil on onionskin paper, a memoir her father had composed of five terrible months in his life. The story began the very day Dr. Baird said goodbye to 5-year-old Mimi and her sister, and permanently left the household. Stunned and bereft all over again, Ms. Baird then spent two decades chasing down the rest of the story, talking to neighbors, colleagues and relatives about long-ago events and obtaining her father’s medical records. Now in her late 70s, a retired medical administrator, she has, with the help of a co-author, woven all this material into “He Wanted the Moon,” an extraordinary Möbius strip of a book. (Read an excerpt.) Its core is the full text of her father’s manuscript, deftly annotated and explained. Around it she layers the voices of caretakers, friends, relatives and medical authorities. Events are revisited and reframed, turned inside out, then right side up again. The book is autobiography, biography, science, history and literature all in one, as instructive as any textbook and utterly impossible to put down. © 2015 The New York Times Company
Link ID: 20600 - Posted: 02.24.2015
By Nathan Seppa Ask anybody — stress is bad news. The negative view of stress has been expressed so consistently that the concept is now built into our vernacular, which is spiced with advice on avoiding it: Take it easy. Calm down. Chill. Of course, a good case of stress comes in handy during an encounter with a grizzly bear on a hiking trail. In that situation, a stress reaction delivers a burst of hormones that revs up the heart and sharpens attention. This automatic response has served humans well throughout evolution, improving our odds of seeing another day. Problems arise, however, when stress becomes a feature of daily life. Chronic stress is the kind that comes from recurring pain, post-traumatic memories, unemployment, family tension, poverty, childhood abuse, caring for a sick spouse or just living in a sketchy neighborhood. Nonstop, low-grade stress contributes directly to physical deterioration, adding to the risk of heart attack, stroke, infection and asthma. Even recovery from cancer becomes harder. Scientists have now identified many of the biological factors linking stress to these medical problems. The evidence centers on nagging inflammation and genetic twists that steer cells off a healthy course, resulting in immune changes that allow ailments to take hold or worsen. Despite the bad rap stress has acquired throughout history, researchers have only recently been able to convince others that it’s dangerous. “It’s taken much more seriously now,” says Janice Kiecolt-Glaser, a clinical psychologist at Ohio State University in Columbus. “In the 1980s, we were still in the dark ages on this stuff.” © Society for Science & the Public 2000 - 2015
By Elizabeth Pennisi Researchers have increased the size of mouse brains by giving the rodents a piece of human DNA that controls gene activity. The work provides some of the strongest genetic evidence yet for how the human intellect surpassed those of all other apes. "[The DNA] could easily be a huge component in how the human brain expanded," says Mary Ann Raghanti, a biological anthropologist at Kent State University in Ohio, who was not involved with the work. "It opens up a whole world of possibilities about brain evolution." For centuries, biologists have wondered what made humans human. Once the human and chimp genomes were deciphered about a decade ago, they realized they could now begin to pinpoint the molecular underpinnings of our big brain, bipedalism, varied diet, and other traits that have made our species so successful. By 2008, almost two dozen computerized comparisons of human and ape genomes had come up with hundreds of pieces of DNA that might be important. But rarely have researchers taken the next steps to try to prove that a piece of DNA really made a difference in human evolution. "You could imagine [their roles], but they were just sort of 'just so' stories,” says Greg Wray, an evolutionary biologist at Duke University in Durham, North Carolina. Wray is particularly interested in DNA segments called enhancers, which control the activity of genes nearby. He and Duke graduate student Lomax Boyd scanned the genomic databases and combed the scientific literature for enhancers that were different between humans and chimps and that were near genes that play a role in the brain. Out of more than 100 candidates, they and Duke developmental neurobiologist Debra Silver tested a half-dozen. They first inserted each enhancer into embryonic mice to learn whether it really did turn genes on. Then for HARE5, the most active enhancer in an area of the brain called the cortex, they made minigenes containing either the chimp or human version of the enhancer linked to a “reporter” gene that caused the developing mouse embryo to turn blue wherever the enhancer turned the gene on. Embryos’ developing brains turned blue sooner and over a broader expanse if they carried the human version of the enhancer, Silver, Wray, and their colleagues report online today in Current Biology. © 2015 American Association for the Advancement of Science
by Sarah Zielinski No one would be shocked to find play behavior in a mammal species. Humans love to play — as do our cats and dogs. It’s not such a leap to believe that, say, a red kangaroo would engage in mock fights. But somehow that behavior seems unlikely in animals other than mammals. It shouldn’t, though. Researchers have documented play behavior in an astonishing range of animals, from insects to birds to mammals. The purpose of such activities isn’t always clear — and not all scientists are convinced that play even exists — but play may help creatures establish social bonds or learn new skills. Here are five non-mammals you may be surprised to find hard at play: Crocodilians Alligators and crocodiles might seem more interested in lurking near the water and chomping on their latest meal, but these frightening reptiles engage in play, Vladimir Dinets of the University of Tennessee in Knoxville reports in the February Animal Behavior and Cognition. Dinets combined 3,000 hours of observations of wild and captive crocodilians with published reports and information gathered from other people who work with the animals. He found examples of all three types of play: Locomotor play: This is movement without any apparent reason or stimulus. Young, captive American alligators, for instance, have been spotted sliding down slopes of water over and over. And a 2.5-meter-long crocodile was seen surfing the waves near a beach in Australia. Object play: Animals like toys, too. A Cuban crocodile at a Miami zoo picked up and pushed around flowers floating in its pool for several days of observation. And like a cat playing with a mouse, a Nile crocodile was photographed as it repeatedly threw a dead hippo into the air. Object play is recognized as so important to crocodilian life “that many zoo caretakers now provide various objects as toys for crocodilians as part of habitat enrichment programs,” Dinets notes. © Society for Science & the Public 2000 - 2015.
Keyword: Development of the Brain
Link ID: 20597 - Posted: 02.21.2015