Chapter 5. The Sensorimotor System

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By BARRY MEIER Addiction experts protested loudly when the Food and Drug Administration approved a powerful new opioid painkiller last month, saying that it would set off a wave of abuse much as OxyContin did when it first appeared. An F.D.A. panel had earlier voted, 11 to 2, against approval of the drug, Zohydro, in part because unlike current versions of OxyContin, it is not made in a formulation designed to deter abuse. Now a new issue is being raised about Zohydro. The drug will be manufactured by the same company, Alkermes, that makes a popular medication called Vivitrol, used to treat patients addicted to painkillers or alcohol. In addition, the company provides financial support to a leading professional group that represents substance abuse experts, the American Society of Addiction Medicine. For some critics, the company’s multiple roles in the world of painkillers is troubling. Dr. Gregory L. Jones, an addiction specialist in Louisville, Ky., said he had long been concerned about financial links between the group and the drug industry, adding that the Zohydro situation amplified those potential conflicts. Dr. Stuart Gitlow, the current president of the American Society of Addiction Medicine, said he had been unaware until now of Alkermes’s involvement with Zohydro. Dr. Gitlow, who is affiliated with Mount Sinai Hospital in New York City, said that the group would seek more information from Alkermes about the situation and then decide what, if anything, to do next. Officials of Alkermes appear to recognize the issue they face. In recent years, the company has been trying to increase sales of Vivitrol, a form of a drug called naltrexone, that is used to treat both alcoholism and opioid addiction. © 2013 The New York Times Company

Keyword: Drug Abuse; Aggression
Link ID: 18931 - Posted: 11.16.2013

by Jessica Griggs, San Diego No practice required. Wouldn't it be great if you could get better at playing sport or hone your piano skills simply by thinking about it? A small pilot study suggests that it might be possible. In the last few years, brain training using computer games that provide neurofeedback – a real-time representation of your brain activity – has become a popular, if controversial, method of enhancing cognitive abilities such as spatial memory, planning and multitasking. It has even been used to help actors get into character. Most of the games aim to enhance activation in a single part of the brain. But motor skills are known to involve two main areas – the premotor cortex and the supplementary motor cortex. Both are involved when people make movements or imagine moving. Brain activity between these regions is known to be less synchronised in people who are poor at motor tasks than in those who excel at them. So to see if brain training could target both areas and improve motor performance, Sook-Lei Liew and her colleagues from the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, recruited eight young adults. The researchers and asked the participants to watch a white circle on a screen while an fMRI machine scanned their brain. When the circle turned into a red triangle, the volunteers were told to move their fingers. This movement caused activation in their premotor cortex and supplementary motor cortex, which in turn moved a bar on the screen. The higher the synchronisation of activity between the two brain areas, the higher the bar went. © Copyright Reed Business Information Ltd.

Keyword: Stroke
Link ID: 18928 - Posted: 11.14.2013

Helen Shen Long used to treat movement disorders, deep-brain stimulation (DBS) is rapidly emerging as an experimental therapy for neuropsychiatric conditions including depression, Tourette’s syndrome, obsessive–compulsive disorder and even Alzheimer’s disease. But despite some encouraging results in patients, it remains largely unknown how the electrical pulses delivered by implants deep within the brain affect neural circuits and change behaviour. Now there is a prototype DBS device that could provide some answers, researchers reported on 10 November at the Society for Neuroscience’s annual meeting in San Diego, California. Called Harmoni, the device is the first DBS implant to monitor electrical and chemical responses in the brain while delivering electrical stimulation. “That’s new data that we haven’t really had access to in humans before,” says Cameron McIntyre, a biomedical engineer at Case Western Reserve University in Cleveland, Ohio, who is not involved in the work. Researchers hope that the device will identify the electrical and chemical signals in the brain that correlate in real time with the presence and severity of symptoms, including the tremors experienced by people with Parkinson’s disease. This information could help to uncover where and how DBS exerts its therapeutic effects on the brain, and why it sometimes fails, says Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minnesota, who is leading the project. The results come at a time of great excitement in the DBS field. Last month, the US government's Defense Advanced Research Projects Agency (DARPA) announced a 5-year, US$70-million initiative to support development of the next generation of therapeutic brain-stimulating technologies. © 2013 Nature Publishing Group,

Keyword: Parkinsons
Link ID: 18922 - Posted: 11.13.2013

Sedentary adults may improve their memory as soon as six weeks after taking up aerobic exercise, a small brain imaging study suggests. Cardiovascular fitness and cognitive performance such as attention seem to improve after six months or more of aerobic exercise in previous aging studies. Now researchers in Texas have found signs of increased regional blood flow in the brain of 37 sedentary adults with an average age of 64 who were randomized to physical training or a control group who had the training after a waiting period. They found a higher resting cerebral blood flow in the brain's anterior cingulate region in the physical training group compared with controls. The anterior cingulate region is associated with better memory functions. The size of this brain region was also larger in another study of "successful cognitive agers" over the age of 80 compared to middle-aged or elderly controls. "A relatively rapid health benefit across brain, memory and fitness in sedentary adults soon after starting to exercise, some gains starting as early as six weeks, could motivate adults to start exercising regularly," the study's lead author, Sandra Bond Champman of the Center for BrainHealth in Dallas and her co-authors concluded in Monday's issue of the journal Frontiers in Aging Neuroscience. "The current findings shed new light on ways exercise promotes cognitive/brain health in aging." The participants all had a physical exam and screening for dementia, early cognitive impairment, depression and IQ before the study began. A noninvasive type of MRI was used to measure brain blood flow before, half way through the 6-week training sessions and at 12 weeks. © CBC 2013

Keyword: Learning & Memory
Link ID: 18920 - Posted: 11.13.2013

Babies born to women who exercised during pregnancy have enhanced brain development compared with babies born to moms who didn’t exercise while they were pregnant, a new Canadian study suggests. The babies of 10 women who did as little as 20 minutes of moderate exercise three times a week during pregnancy showed more advanced brain activity when they were tested at eight to 12 days old than the babies of eight women who did not exercise during pregnancy, reported University of Montreal researcher David Ellemberg and his colleagues at the Neuroscience 2013 conference in San Diego on Sunday. “We are optimistic that this will encourage women to change their health habits, given that the simple act of exercising during pregnancy could make a difference for their child's future,” Ellemberg said in a statement. The women in the study were randomly assigned to an exercise group or a sedentary group at the beginning of their second trimester. Those in the exercise group had to spend at least 20 minutes three times a week doing exercise intense enough to lead to at least a slight shortness of breath. After their babies were born, the researchers tested them by placing a cap of electrodes on the babies' heads and then playing novel sounds while they slept. They measured the electrical response of the babies' brains to see how well they could distinguish between different sounds. The researchers found that the babies in the exercise group produced signals associated with more mature brains. The researchers said they plan to test the children’s cognitive, motor and language development at age one to see if there are lasting effects. © CBC 2013

Keyword: Development of the Brain
Link ID: 18916 - Posted: 11.12.2013

By PAM BELLUCK It is probably no accident that the pivotal object in Martin Cruz Smith’s newest detective thriller, “Tatiana,” is a notebook nobody can read. Early on, Mr. Smith worried that his novel, being published Tuesday by Simon & Schuster, would be unreadable too — or wouldn’t be written at all. Author of the 1981 blockbuster “Gorky Park” and many acclaimed books since, Mr. Smith writes about people who uncover and keep secrets. But for 18 years, he has had a secret of his own. In 1995, he received a diagnosis of Parkinson’s disease. But he kept it hidden, not only from the public, but from his publisher and editors. He concealed it, although for years, tremors and stiffness have kept him from taking detailed notes and sketching people, places and objects for his research — and even as he became unable to type the words he needed to finish his 2010 best seller “Three Stations.” “I didn’t want to be judged by that,” Mr. Smith, 71, explained recently in his light-filled Victorian home north of San Francisco. “Either I’m a good writer or I’m not. ‘He’s our pre-eminent Parkinson’s writer.’ Who needs that?” In talking about his Parkinson’s odyssey, including a relatively new but promising treatment, Mr. Smith is opening a window on the still incurable disorder affecting four million people worldwide, a disease that is becoming increasingly prevalent as baby boomers age. His experience reflects a common desire to conceal often-stigmatizing symptoms, like shaking, slowness, and rigidity. (He mostly didn’t mind his Parkinsonian hallucinations: a black cat in his lap, whirlwinds spiraling from computer keys, a butler, a British military officer in full regalia. “Having hallucinations for a fiction writer is redundant,” he said.) Copyright 2013 The New York Times Company

Keyword: Parkinsons
Link ID: 18914 - Posted: 11.12.2013

by Ashley Yeager The compound that gives mold its musty smell can cause changes in fruit flies’ brains that mimic those of patients with Parkinson’s disease. Scientists do not know the exact cause of Parkinson’s disease, but studies have shown that exposure to human-made chemicals may be a risk factor for developing the movement disorder. Now researchers have found that the chemical 1-octen-3-ol, which mold naturally emits, kills flies’ brain cells that transmit dopamine, a compound involved in controlling movement. The mold molecule also reduces dopamine levels in the flies’ brains. In experiments with human cells, the mold chemical also blocked the cells from taking in dopamine, researchers report November 11 in the Proceedings of the National Academy of Sciences. The results offer insight into cases of movement problems that doctors have associated with fungi exposure, the scientists say. © Society for Science & the Public 2000 - 2013

Keyword: Movement Disorders; Aggression
Link ID: 18911 - Posted: 11.12.2013

Sarah DeWeerdt Parts of the brain that process vision and control movements are poorly connected in children with autism, according to results presented Saturday at the 2013 Society for Neuroscience annual meeting in San Diego. In addition to the social deficits that are a core feature of autism, children with the disorder often have clumsy movements. Studies have also found that people with autism have trouble imitating others. The new study uncovers patterns of brain activity suggesting all three of these deficits may be related. The researchers used functional magnetic resonance imaging (fMRI) to measure resting-state activation — brain activity that occurs while individuals are resting quietly in the scanner — in 45 children with autism and 45 controls. Parts of the brain that tend to activate and deactivate together during this procedure are said to be functionally connected. The researchers zeroed in on two sets of brain structures involved in motor activity. One of them, the ventral motor component, includes parts of the cortex, the thalamus and lobule 6 of the cerebellum. They also focused on three areas of the brain involved in visual processing. The most interesting is a region at the back of the brain responsible for complex interpretation of visual information. © Copyright 2013 Simons Foundation

Keyword: Autism; Aggression
Link ID: 18906 - Posted: 11.11.2013

Roughly a year ago, I found myself at an elegant dinner party filled with celebrities and the very wealthy. I am a young professor at a major research university, and my wife and I were invited to mingle and chat with donors to the institution. To any outside observer, my career was ascendant. Having worked intensely and passionately at science for my entire adult life, I had secured my dream job directing an independent neuroscience research laboratory. I was talking to a businessman who had family members affected by a serious medical condition. He turned to me and said: “You're a neuroscientist. What do you know about Parkinson's disease?” My gaze darted to catch the eyes of my wife, but she was involved in another conversation. I was on my own, and I paused to gather my thoughts before responding. Because I had a secret. It was a secret that I hadn't yet told any of my colleagues: I have Parkinson's. I am still at the beginning of my fascinating, frightening and ultimately life-affirming journey as a brain scientist with a disabling disease of the brain. Already it has given me a new perspective on my work, it has made me appreciate life and it has allowed me to see myself as someone who can make a difference in ways that I never expected. But it took a bit of time to get here. The first signs I remember the first time I noticed that something was wrong. Four years ago, I was filling out a mountain of order forms for new lab equipment. After a few pages, my hand became a quaking lump of flesh and bone, locked uselessly in a tense rigor. A few days later, I noticed my walk was changing: rather than swinging my arm at my side, I held it in front of me rigidly, even grabbing the bottom edge of my shirt. I also had an occasional twitch in the last two fingers of my hand. © 2013 Nature Publishing Group

Keyword: Parkinsons
Link ID: 18896 - Posted: 11.08.2013

Most of us don’t think twice when we extend our arms to hug a friend or push a shopping cart—our limbs work together seamlessly to follow our mental commands. For researchers designing brain-controlled prosthetic limbs for people, however, this coordinated arm movement is a daunting technical challenge. A new study showing that monkeys can move two virtual limbs with only their brain activity is a major step toward achieving that goal, scientists say. The brain controls movement by sending electrical signals to our muscles through nerve cells. When limb-connecting nerve cells are damaged or a limb is amputated, the brain is still able to produce those motion-inducing signals, but the limb can't receive them or simply doesn’t exist. In recent years, scientists have worked to create devices called brain-machine interfaces (BMIs) that can pick up these interrupted electrical signals and control the movements of a computer cursor or a real or virtual prosthetic. So far, the success of BMIs in humans has been largely limited to moving single body parts, such as a hand or an arm. Last year, for example, a woman paralyzed from the neck down for 10 years commanded a robotic arm to pick up and lift a piece of chocolate to her mouth just by thinking about it. But, "no device will ever work for people unless it restores bimanual behaviors,” says neuroscientist Miguel Nicolelis at Duke University in Durham, North Carolina, senior author of the paper. "You need to use both arms and hands for the simplest tasks.” In 2011, Nicolelis made waves by announcing on The Daily Show that he is developing a robotic, thought-controlled "exoskeleton" that will allow paralyzed people to walk again. Further raising the stakes, he pledged that the robotic body suit will enable a paralyzed person to kick a soccer ball during the opening ceremony of the 2014 Brazil World Cup. (Nicolelis is Brazilian and his research is partly funded by the nation’s government.) © 2013 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 18888 - Posted: 11.07.2013

By DONALD G. McNEIL Jr. The World Health Organization has approved a new vaccine for a strain of encephalitis that kills thousands of children and leaves many survivors with permanent brain damage. The move allows United Nations agencies and other donors to buy it. The disease, called Japanese encephalitis or brain fever, is caused by a mosquito-transmitted virus that can live in pigs, birds and humans. Less than 1 percent of those infected get seriously ill, but it kills up to 15,000 children a year and disables many more. Up to four billion people, from southern Russia to the Pacific islands, are at risk; it is more prevalent near rice paddies. There is no cure. The low-cost vaccine, approved last month, is the first authorized by the agency for children and the first Chinese-made vaccine it has approved. It is made by China National Biotec Group and was tested by PATH, a nonprofit group in Seattle with funding from the Bill and Melinda Gates Foundation. Dr. Margaret Chan, W.H.O.’s director-general, said she hoped that approval would encourage other vaccine makers from China and elsewhere to enter the field. China had given the vaccine domestically to 200 million children over many years but had never sought W.H.O. approval. India, which previously bought 88 million doses from China, launched the first locally produced version last month. © 2013 The New York Times Company

Keyword: Miscellaneous
Link ID: 18872 - Posted: 11.05.2013

By JANE E. BRODY Marijuana has been used medically, recreationally and spiritually for about 5,000 years. Known botanically as cannabis, it has been called a “crude drug”: marijuana contains more than 400 chemicals from 18 chemical families. More than 2,000 compounds are released when it is smoked, and as with tobacco, there are dangers in smoking it. Medical marijuana clinics operate in 20 states and the District of Columbia, and its recreational use is now legal in Colorado and Washington. A Gallup poll conducted last month found that 58 percent of Americans support the legalization of marijuana. Yet researchers have been able to do relatively little to test its most promising ingredients for biological activity, safety and side effects. The main reason is marijuana’s classification by Congress in 1970 as an illegal Schedule I drug, defined as having a potential for abuse and addiction and no medical value. American scientists seeking clarification of marijuana’s medical usefulness have long been stymied by this draconian classification, usually reserved for street drugs like heroin with a high potential for abuse. Dr. J. Michael Bostwick, a psychiatrist at the Mayo Clinic in Rochester, Minn., said the classification was primarily political and ignored more than 40 years of scientific research, which has shown that cellular receptors for marijuana’s active ingredients are present throughout the body. Natural substances called cannabinoids bind to them to influence a wide range of body processes. In a lengthy report entitled “Blurred Boundaries: The Therapeutics and Politics of Medical Marijuana,” published last year in Mayo Clinic Proceedings, Dr. Bostwick noted that the so-called endocannabinoid system has an impact on the “autonomic nervous system, immune system, gastrointestinal tract, reproductive system, cardiovascular system and endocrine network.” Copyright 2013 The New York Times Company

Keyword: Drug Abuse; Aggression
Link ID: 18866 - Posted: 11.04.2013

If you were stung by a bark scorpion, the most venomous scorpion in North America, you’d feel something like the intense, painful jolt of being electrocuted. Moments after the creature flips its tail and injects venom into your skin, the intense pain would be joined by a numbness or tingling in the body part that was stung, and you might experience a shortness of breath. The effect of this venom on some people—small children, the elderly or adults with compromised immune systems—can even trigger frothing at the mouth, seizure-like symptoms, paralysis and potentially death. Based solely on its body size, the four-inch-long furry grasshopper mouse should die within minutes of being stung—thanks to the scorpion’s venom, which causes temporary paralysis, the muscles that allow the mouse to breathe should shut down, leading to asphyxiation—so you’d think the rodent would avoid the scorpions at all costs. But if you put a mouse and a scorpion in the same place, the rodent’s reaction is strikingly brazen. If stung, the four-inch-long rodent might jump back for a moment in surprise. Then, after a brief pause, it’ll go in for the kill and devour the scorpion piece by piece: This predatory behavior isn’t the result of remarkable toughness. As scientists recently discovered, the mouse has evolved a particularly useful adaptation: It’s immune to both the pain and paralytic effects that make the scorpion’s venom so toxic. Although scientists long knew that the mouse, native to the deserts of the American Southwest, preys upon a range of non-toxic scorpions, “no one had ever really asked whether they attack and kill really toxic scorpions,” says Ashlee Rowe of Michigan State University, who led the new study published today in Science.

Keyword: Pain & Touch; Aggression
Link ID: 18839 - Posted: 10.28.2013

Who would win in a fight: a bark scorpion or a grasshopper mouse? It seems like an easy call. The bark scorpion (Centruroides sculpturatus) delivers one of the most painful stings in the animal kingdom—human victims have compared the experience to being branded. The 25-gram grasshopper mouse (Onychomys torridus) is, well, a mouse. But as you can see in the video above, grasshopper mice routinely kill and eat bark scorpions, blissfully munching away even as their prey sting them repeatedly (and sometimes right in the face). Now, scientists have discovered why the grasshopper mice don’t react to bark scorpion stings: They simply don’t feel them. Evolutionary neurobiologist Ashlee Rowe at the University of Texas, Austin, has been studying the grasshopper mice’s apparent superpower since she was in graduate school. For the new study, she milked venom from nearly 500 bark scorpions and started experimenting. When she injected the venom into the hind paws of regular laboratory mice, the mice furiously licked the site for several minutes. But when she injected the same venom into grasshopper mice, they licked their paws for just a few seconds and then went about their business, apparently unfazed. In fact, the grasshopper mice appeared to be more irritated by injections of the saline solution Rowe used as a control. Rowe knew that grasshopper mice weren’t entirely impervious to pain—they reacted to injections of other painful chemicals such as formalin, just not the bark scorpion venom. To find out what was going on, she and her team decided to determine how the venom affects the grasshopper mouse’s nervous system, in particular the parts responsible for sensing pain. © 2013 American Association for the Advancement of Science

Keyword: Pain & Touch; Aggression
Link ID: 18838 - Posted: 10.26.2013

By JAMES GORMAN Worldwide, 100,000 people have electrical implants in their brains to treat the involuntary movements associated with Parkinson’s disease, and scientists are experimenting with the technique for depression and other disorders. But today’s so-called deep brain stimulation only treats — it does not monitor its own effectiveness, partly because complex ailments like depression do not have defined biological signatures. The federal Defense Advanced Research Projects Agency, known as Darpa, announced Thursday that it intended to spend more than $70 million over five years to jump to the next level of brain implants, either by improving deep brain stimulation or by developing new technology. Justin Sanchez, Darpa program manager, said that for scientists now, “there is no technology that can acquire signals that can tell them precisely what is going on with the brain.” And so, he said, Darpa is “trying to change the game on how we approach these kinds of problems.” The new program, called Systems-Based Neurotechnology and Understanding for the Treatment of Neuropsychological Illnesses, is part of an Obama administration brain initiative, announced earlier this year, intended to promote innovative basic neuroscience. Participants in the initiative include Darpa, as well as the National Institutes of Health and the National Science Foundation. The announcement of Darpa’s goal is the first indication of how that research agency will participate in the initiative. The money is expected to be divided among different teams, and research proposals are now being sought. Darpa’s project is partly inspired by the needs of combat veterans who suffer from mental and physical conditions, and is the first to invest directly in researching human illness as part of the brain initiative. © 2013 The New York Times Company

Keyword: Depression; Aggression
Link ID: 18835 - Posted: 10.26.2013

By NELSON GRAVES Six years ago I suffered a stroke that forced me to relearn how to walk. The other day I ran a half-marathon. Strokes strike with stealth, but for me it was not entirely a surprise. During a physical in Milan in 2007, the doctor listened to my heart, then ordered an electrocardiogram. “Fair enough,” I reassured myself. “I’m 52 years old, and it’s no use taking anything for granted.” The nurse furrowed her brow as she studied the first read-out, then conducted a second, longer EKG. I put my shirt back on and returned to the doctor’s office. “I have some news for you,” he said. “You have atrial fibrillation. AF for short.” He wrote down the two words and explained they meant an irregular beating of the heart’s upper chambers. “It’s not life threatening. But it increases the risk of stroke six-fold.” I was too young to have a stroke. “I work 12-hour days, play squash three times a week and haven’t missed a day of work in 24 years,” I said. My attention piqued, I could now hear my heart’s irregular beat as I lay my head on my pillow. That must explain the dizziness when I get up at night to go to the bathroom. Or the fatigue at the end of a squash match. So when, on a September afternoon in Tokyo, my head began to spin wildly and I could hardly speak, I knew what was happening. After an ambulance ride to the hospital and an M.R.I., I heard the doctor say, “You’ve had a cerebral embolism.” That would be a stroke. Copyright 2013 The New York Times Company

Keyword: Stroke
Link ID: 18833 - Posted: 10.26.2013

People with Parkinson's disease are dancing at the National Ballet School as part of a study into how learning dance moves can change the brain. Anecdotally, learning to dance seems to improve motor skills in the short-term among people with Parkinson's disease, a neurological disorder that interferes with gait and balance. As part of a 12-week program, 20 people with Parkinson's disease are taking weekly dance classes at the National Ballet School in Toronto. The classes began in September. The research team is led by neuroscientist Prof. Joseph DeSouza of York University's Faculty of Health and National Ballet School instructor Rachel Bar. The volunteers are also getting a series of functional MRI scans to help researchers understand how the brain reacts and learns. "We know that balance can improve and gait can improve and even there's social benefits but we want to see why that's happening, how is it happening? To do that, we're looking inside the brain," Bar said. People aren't able to dance in scanner but they are asked to visualize the dance while listening to the accompanying music. "If you visualize a dance, theoretically you're using almost all the same neural circuitry as if you were doing it," DeDouza said. The hypothesis is that the brain of someone with Parkinson's may develop new paths around damaged areas if stimulated by the movement of dance. © CBC 2013

Keyword: Parkinsons
Link ID: 18826 - Posted: 10.23.2013

by NPR Staff Soon you'll be able to direct the path of a cockroach with a smartphone and the swipe of your finger. Greg Gage and his colleagues at Backyard Brains have developed a device called the that lets you control the path of an insect. It may make you squirm, but Gage says the device could inspire a new generation of neuroscientists. "The sharpest kids amongst us are probably going into other fields right now. And so we're kind of in the dark ages when it comes to neuroscience," he tells NPR's Arun Rath. He wants to get kids interested in neuroscience early enough to guide them toward that career path. And a cyborg cockroach might be the inspiration. "The neurons in the insects are very, very similar to the neurons inside the human brain," Gage says. "It's a beautiful way to just really understand what's happening inside your brain by looking at these little insects." The idea was spawned by a device the Backyard Brain-iacs developed called , which is capable of amplifying real living neurons. Insert a small wire into a cockroach's antennae, and you can hear the sound of actual neurons. "Lining the inside of the cockroach are these neurons that are picking up touch or vibration sensing, chemical sensing," Gage says. "They use it like a nose or a large tongue, their antennas, and they use it to sort of navigate the world. "So when you put a small wire inside of there, you can actually pick up the information as it's being encoded and being sent to the brain." With the RoboRoach device and smartphone app, you can interact with the antennae to influence the insect's behavior. ©2013 NPR

Keyword: Robotics
Link ID: 18819 - Posted: 10.22.2013

Henry Astley In the Mark Twain story The Celebrated Jumping Frog of Calaveras County, a frog named Daniel Webster "could get over more ground at one straddle than any animal of his breed you ever see." Now, scientists have visited the real Calaveras County in hopes of learning more about these hopping amphibians. They’ve found that what they see in the lab doesn’t always match the goings-on in the real world. If you wanted to know how far the bullfrog Rana catesbeiana could jump, the scientific literature would give you one answer: 1.295 meters, published in Smithsonian Contributions to Zoology in 1978. If you looked at the Guinness Book of World Records, though, you'd find a different answer. In 1986, a bullfrog called Rosie the Ribeter covered 6.55 meters in three hops. If you divide by three, at least one of those hops had to be no shorter than 2.18 meters—about four bullfrog body lengths more than the number in the scientific paper. The disparity matters. If bullfrogs can hop only 1.3 meters, they have enough power in their muscles to pull off the jump without any other anatomical help. But if they can jump farther, they must also be using a stretchy tendon to power their hops—an ability that other frogs have but that researchers thought bullfrogs had lost. These particular amphibians, scientists speculated, might have made some kind of evolutionary tradeoff that shortened their jumps but enabled them to swim better in the water, where they spend much of their lives. © 2013 American Association for the Advancement of Science

Keyword: Miscellaneous
Link ID: 18800 - Posted: 10.17.2013

By Lary C. Walker Clumps of proteins twisted into aberrant shapes cause the prion diseases that have perplexed biologists for decades. The surprises just keep coming with a new report that the simple clusters of proteins responsible for Mad Cow and other prions diseases may, without help from DNA or RNA, be capable of changing form to escape the predations of drugs that target their eradication. Prion drug resistance could be eerily similar to that found in cancer and HIV—and may have implications for drug development for Alzheimer’s and Parkinson’s, neurodegenerative diseases also characterized by misfolded proteins. Prion diseases include scrapie, chronic wasting disease and bovine spongiform encephalopathy (mad cow disease) in nonhuman species, and Creutzfeldt-Jakob disease and fatal insomnia in humans. They are unusual in that they can arise spontaneously, as a result of genetic mutations, or, in some instances, through infection. Remarkably, the infectious agent is not a microbe or virus, but rather the prion itself, a clump of proteins without genetic material. The noxious agents originate when a normally generated protein – called the prion protein – mistakenly folds into a stable, sticky, and potentially toxic shape. When the misfolded protein contacts other prion protein molecules, they too are corrupted and begin to bind to one another. In the ensuing chain reaction, the prions grow, break apart, and spread; within the nervous system, they relentlessly destroy neurons, ultimately, and invariably, leading to death. © 2013 Scientific American

Keyword: Prions; Aggression
Link ID: 18799 - Posted: 10.17.2013