by Robert F. Service According to George Bernard Shaw: "The most intolerable pain is produced by prolonging the keenest pleasure." Not to be picky George, but actually both sensations result from the activity of a diverse family of proteins on the surface of cells. This year's Nobel Prize in chemistry was awarded to two Americans—Robert Lefkowitz of Duke University in Durham, North Carolina, and Brian Kobilka of Stanford University School of Medicine in Palo Alto, California—who revealed the inner workings of these proteins, which also orchestrate a variety of things such as the way we see, smell, taste, feel, and fight infections. The notion that a single family of proteins was responsible for so many different physiological processes was far from evident early on. One hint came at the end of the 19th century, when scientists studying the effects of the hormone adrenaline discovered that it had different effects in various parts of the body. It made heart rate and blood pressure increase, but it decreased digestive activity and caused pupils to relax. One idea was that proteins called receptors on different cells somehow captured adrenaline molecules and either ferried the hormone into cells or transferred a message inside to trigger a response. In the 1940s, an American biologist named Raymond Ahlquist made enough progress to conclude that there must be two types of adrenaline receptors, one that caused smooth muscle cells to contract, and the other that stimulated the heart. © 2010 American Association for the Advancement of Science

Keyword: Pain & Touch; Aggression
Link ID: 17354 - Posted: 10.11.2012

By Tina Hesman Saey The 2012 Nobel Prize in physiology or medicine was awarded for the discovery that adult cells can be reprogrammed, as scientists did to these neurons, created from skin cells reprogrammed into a type of primordial stem cell and then coaxed into brain cells that control movement.G. Croft and M. Weygandt/The Cell: An Image Library Two scientists who showed that a cell's fate is reversible have won the 2012 Nobel Prize in physiology or medicine. The Nobel committee announced October 8 that John Gurdon and Shinya Yamanaka are being honored for showing that cells once thought to be locked into a specific identity could remember and revert to the supremely flexible state they have in an early embryo. Gurdon’s 1962 work forever changed the view that adult cells are stuck in their fate. In a series of experiments, he transplanted the nucleus — the cellular compartment that contains DNA — from an intestinal cell of an adult frog into a frog egg cell from which the nucleus had been removed. The cell developed into a normal tadpole, demonstrating that DNA contains all the information necessary to make an embryo. More than four decades later, Yamanaka, of Kyoto University in Japan, changed the debate over stem cells when he created induced pluripotent stem cells, which are capable of becoming nearly any cell in the body. He was trying to understand the factors that make stem cells isolated from embryos so malleable; many genes seemed to be involved. Yamanaka used viruses to insert combinations of candidate genes into skin cells, and found that only four genes are required to turn a mouse skin cell into a stem cell. The technique has since been used to convert adult human cells into embryonic-like cells and even to convert skin cells directly into heart or brain cells. © Society for Science & the Public 2000 - 2012

Keyword: Stem Cells; Aggression
Link ID: 17346 - Posted: 10.09.2012

Two pioneers of stem cell research have shared the Nobel prize for medicine or physiology. John Gurdon from the UK and Shinya Yamanaka from Japan were awarded to prize for transforming specialised cells into stem cells.

Keyword: Stem Cells; Aggression
Link ID: 17342 - Posted: 10.08.2012

By Katherine Harmon A bite from the black mamba snake (Dendroaspis polylepis) can kill an adult human within 20 minutes. But mixed in with that toxic venom is a new natural class of compound that could be used to help develop new painkillers. Named “mambalgins,” these peptides block acute and inflammatory pain in mice as well as morphine does, according to a new study. Researchers, led by Sylvie Diochot, of the Institute of Molecular and Cellular Pharmacology at Nice University, Sophia Antipolis in France, purified the peptides from the venom and profiled the compounds’ structure. They then were able to test the mambalgins in strains of mice with various genetic tweaks to their pain pathways. Diochot and her colleagues determined that the mambalgins work by blocking an as-yet untargeted set of neurological ion channels associated with pain signals. The findings were published online October 3 in Nature (Scientific American is part of Nature Publishing Group). As a bonus, mambalgins did not have the risky side effect of respiratory depression that morphine does. And the mice developed less tolerance to them over time than is typical with morphine. Experimenting with the newfound compounds should also help researchers learn more about the mechanisms that drive pain. As the researchers noted in their paper, “It is essential to understand pain better to develop new analgesics. The black mamba peptides discovered here have the potential to address both of these aims.” © 2012 Scientific American,

Keyword: Pain & Touch; Aggression
Link ID: 17333 - Posted: 10.04.2012

By ANDREW POLLACK An experimental drug preserved and even improved the walking ability of boys with Duchenne muscular dystrophy in a clinical trial, raising hopes that the first effective treatment for the disease may be on the horizon. Boys with the disease who received the highest dose of the drug had a slightly improved ability to walk after 48 weeks of treatment, the drug’s developer, Sarepta Therapeutics, announced Wednesday. By contrast, the boys who received a placebo suffered a sharp decline in how well they could walk. The drug, called eteplirsen, also appeared to restore levels of the crucial protein that muscular dystrophy patients lack to about half of normal levels, Sarepta said. “I think this changes the entire playing field for muscular dystrophy,” said Dr. Jerry R. Mendell, director of the gene therapy and muscular dystrophy programs at Nationwide Children’s Hospital in Columbus, Ohio, and the lead investigator in the trial. There are many caveats. The trial had only 12 patients, with only four receiving the high dose and four the placebo, and the data has not been reviewed by experts. It is also unclear how long the effects of the drug would last or if safety issues would arise with longer treatment. Also, eteplirsen would be appropriate for only about 13 percent to 15 percent of Duchenne patients, those with the particular genetic mutation the drug is meant to counteract. However, a similar approach might work for some other mutations. © 2012 The New York Times Company

Keyword: Movement Disorders; Aggression
Link ID: 17331 - Posted: 10.04.2012

By PAUL CHRISTOPHER, M.D. “I’m addicted to painkillers,” J., a thickset construction worker, told me on a recent afternoon in the emergency room, his wife at his side. Two years before, after months of pain, stiffness and swelling in his hands and neck, his primary physician had diagnosed rheumatoid arthritis and had prescribed three medications: two to slow the disease and one, oxycodone, for pain. Bolstered by the painkiller, J. had felt more limber and energetic than he had in years. “I could finally keep up with the other guys,” he told me. He worked harder, and his pain worsened. His primary physician increased the oxycodone dose. Soon, J. was looking forward more to the buzz than to the relief the pills brought. He went to see two other physicians who, unaware that he was double-dipping, prescribed similar medications. When a co-worker offered to sell him painkillers directly, J.’s use spiraled out of control. By the time I saw him, he was taking dozens of pills a day, often crushing and snorting them to speed the onset of his high. With remarkable candor, he described how the drugs had marred every facet of his life — from days of missed work to increasing debt, deteriorating health and marital strain. But when I listed the treatment options that might help, J. shook his head, looked from me to his wife, and got up. “I’m all set,” he said, holding up his hands. Then he walked out of the room. Despair fell on his wife’s face. “Please,” she said, grabbing my arm, “you can’t let him leave.” Copyright 2012 The New York Times Company

Keyword: Drug Abuse; Aggression
Link ID: 17327 - Posted: 10.03.2012

By Gary Stix 14 inSharHuntington’ disease, which killed folk singer Woody Guthrie, seems to put into overdrive the main chemical that turns on brain cells, ultimately leading to their death. The normal function of the neurotransmitter glutamate, the chemical overproduced in Huntington’s, is also intimately involved with learning. Researchers from Ruhr University and the University of Dortmund in Germany have been intrigued by the question of whether the neurodegeneration initiated by glutamate in this genetic disorder is all bad. Is it simply  burning out brain circuits? Or might an excess of the chemical also help presymptomatic carriers of the Huntington’s gene or even patients with the disease itself,  learn some things faster or better? “Neurotransmission causes cell death but we know from the vast amount of literature that learning processes very much depend on glutamate neurotransmission; so there may be two effects of one and the same process,” says Christian Beste of Ruhr University. “On the one hand this process may lead to neurodegeneration. But on the other hand, it may augment a cognitive process that depends on glutamate transmission.” Beste is the lead author on a paper published this month in Current Biology that found that those who have the genetic mutation for Huntington’s but who have yet to develop inevitable symptoms of the disease perform better on a learning task than a control group that lacks the mutation. The 29 Huntington’s gene carriers learned to detect twice as fast as the 45 controls a change in brightness of a small bar as its orientation on a computer screen altered. In fact, the Huntington’s carriers with the most pronounced mutations—the number of repetitions of a short DNA segment determines how early disease onset occurs—logged the best performance. © 2012 Scientific American,  

Keyword: Huntingtons
Link ID: 17311 - Posted: 09.29.2012

By Sandra G. Boodman, The 80th birthday party for Josephine van Es marked two milestones, only one of which was apparent at the time. Held in November 2004 at her daughter’s house in Rehoboth Beach, Del., the event was a celebration of her longevity, good health and loving family. It also marked one of the last times van Es can remember feeling well and not beset by the pain that developed soon afterward and has left the inside of her mouth feeling perpetually scalded and with a constant metallic taste. “It’s awful,” said van Es, 87, who says the burning is worse than the taste, which she likens to “sucking on a penny.” Her daughter Karen van Es says that her mother’s problem has taken a toll on both their lives. For nearly eight years, she has taken time from her job at a Northern Virginia veterinary clinic to ferry her mother, who lives independently in a condominium in Lewes, Del., to doctors in Delaware, Philadelphia and Washington. She also has contacted specialists in Florida and Canada hoping one would propose an effective remedy for an ailment that took more than a year to diagnose and has so far eluded treatment. “She tells me, ‘I just feel rotten all the time,’ ” said Karen van Es, 63, an only child who speaks to her mother every day and sees her often. “My mother has lost confidence as a result of this,” Karen van Es said, adding that she often feels helpless and frustrated about not being able to do more. © 1996-2012 The Washington Post

Keyword: Chemical Senses (Smell & Taste); Aggression
Link ID: 17305 - Posted: 09.26.2012

By GRETCHEN REYNOLDS Can you improve your body’s ability to remember by making it move? That rather odd-seeming question stimulated researchers at the University of Copenhagen to undertake a reverberant new examination of just how the body creates specific muscle memories and what role, if any, exercise plays in the process. To do so, they first asked a group of young, healthy right-handed men to master a complicated tracking skill on a computer. Sitting before the screen with their right arm on an armrest and a controller similar to a joystick in their right hand, the men watched a red line squiggle across the screen and had to use the controller to trace the same line with a white cursor. Their aim was to remain as close to the red squiggle as possible, a task that required input from both the muscles and the mind. The men repeated the task multiple times, until the motion necessary to track the red line became ingrained, almost automatic. They were creating a short-term muscle memory. The term “muscle memory” is, of course, something of a misnomer. Muscles don’t make or store memories. They respond to signals from the brain, where the actual memories of any particular movement are formed and filed away. But muscle memory — or “motor memory,” as it is more correctly referred to among scientists — exists and can be quite potent. Learn to ride a bicycle as a youngster, abandon the pastime and, 20 years later, you’ll be able to hop on a bicycle and pedal off. Copyright 2012 The New York Times Company

Keyword: Learning & Memory
Link ID: 17304 - Posted: 09.26.2012

By PAULINE W. CHEN, M.D. Recounting her father’s struggle with cancer was difficult for the young woman, even several years after his death. He’d endured first surgery and then chemotherapy and radiation, she told me, and the cancer had gone into remission. He was thrilled, but the aggressive treatment left him with chronic, debilitating pain. Once active, he struggled to get around in his own home. “It wasn’t the cancer that got him,” the daughter said. “It was the pain.” Her father had turned to all of his doctors, with little relief. His surgeon had looked at his operative wounds, pronounced them well healed, then stated that they were in no way responsible for his disability. Both his cancer doctor and his radiation doctor congratulated him on being in remission but then declined to prescribe pain medications since they were no longer treating him and couldn’t provide ongoing follow-up and dosing guidance. His primary care doctor listened intently to his descriptions of his limitations, but then prescribed only small amounts of pain meds that offered fleeting relief at best. “I’ll never forget what my father had to go through,” she said, weeping. “I wouldn’t wish this on anyone.” I wish I could have reassured her that her father’s case was unusual. Sadly, according to a new study in The Journal of Clinical Oncology, a significant percentage of cancer patients continue to suffer from pain as her father did. Copyright 2012 The New York Times Company

Keyword: Pain & Touch; Aggression
Link ID: 17300 - Posted: 09.26.2012

By James Gallagher Health and science reporter, BBC News Up to a million people in the UK have "completely preventable" severe headaches caused by taking too many painkillers, doctors have said. They said some were trapped in a "vicious cycle" of taking pain relief, which then caused even more headaches. The warning came as part of the National Institute for Health and Clinical Excellence's (NICE) first guidelines for treating headaches. It is also recommending acupuncture in some circumstances. "Medication overuse headaches" feel the same as other common headaches or migraines. There is no definitive UK data on the incidence of the condition, but studies in other countries suggest 1-2% of people are affected, while the World Health Organization says figures closer to 5% have been reported. While painkillers would be many people's instant response, they could be making sufferers feel even worse. Prof Martin Underwood, from Warwick Medical School, who led the NICE panel, said: "This can end up getting into a vicious cycle where your headache gets worse, so you take more painkillers, so your headache gets worse and this just becomes worse and worse and worse. BBC © 2012

Keyword: Pain & Touch
Link ID: 17277 - Posted: 09.19.2012

In May, my six-year-old daughter, Julia, smashed into our front door handle and got a deep, bloody gash in her forehead. We rushed her, head wrapped like a tiny mummy, to the medical center at MIT, where we generally go for pediatric care. Julia wept while the nurse cleaned and examined her lacerated skin. After a short exam, she sent us to the emergency department at Children’s Hospital Boston for stitches. “How bad is that, generally?” I asked, having never experienced suturing either for myself or my cautious, risk-averse, older daughter. “It can be traumatic,” the nurse said. Julia cried, “I don’t want stitches.” It’s a large needle, but Julia is too busy coloring to notice. So I braced myself for the worst: an endless wait and nerve-wracking bustle; screaming, germ-laden children and brusque, end-of-shift staff. But more than anything, I dreaded the inevitable pain in store for my small child with the deep cut. (I know, kids get banged up on the path to adulthood and some pain is unavoidable. Still, when bloody heads are involved, I tend to overreact.) Indeed, I was in full Mama Bear mode when into our exam room strode Dr. Baruch Krauss, the attending physician that evening. Copyright Trustees of Boston University

Keyword: Pain & Touch; Aggression
Link ID: 17276 - Posted: 09.19.2012

By Jorge Cham and Dwayne Godwin [Graphic novel format.] Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2012 Scientific American,

Keyword: Pain & Touch
Link ID: 17264 - Posted: 09.17.2012

Daniel Cressey Rabbits are the latest focus of work seeking to measure animal discomfort by assessing facial expressions. Researchers working with animals often find it difficult to scientifically assess when their study subjects are in pain. Traditional methods rely on after-the-fact measurements involving weight loss or food and water consumption, or on subjective judgements such as how an animal moves. In an attempt to make pain assessment more scientific, geneticist Jeffrey Mogil at McGill University in Montreal, Canada, and his colleagues developed the 'mouse grimace scale', which was published in Nature Methods1 in May 2010 (see 'Mice pull pained expressions'). The scale relies on the scoring of five ‘action units’ — such as narrowing of the eyes and bulging of the cheeks — between zero (not present) and two (obviously present), with the combined score indicating total pain. The scale rapidly caught on among veterinarians to assess post-operative pain. “I’m surprised how quickly it was adopted as a practical thing to use in real-time for animal care,” says Mogil. Matthew Leach, who researches animal welfare at Newcastle University, UK, and led the work in rabbits, has been working on facial expressions of pain in various animals since the original mouse grimace scale came out. "The only way you can alleviate pain is to be able to identify it, and to understand how much pain an animal is in," he says. "There is a broad interest in grimace scales,” he notes, adding that compared with traditional models, “I would argue it’s potentially better and faster in many circumstances”. © 2012 Nature Publishing Group

Keyword: Pain & Touch
Link ID: 17238 - Posted: 09.10.2012

by Andy Coghlan Muscles that burn energy without contracting have yielded new clues about how the body retains a constant temperature – and they may provide new targets for combating obesity. Traditionally, the body's main thermostat was thought to be brown fat. It raids the body's white fat stores in cold conditions to burn energy and keep the body warm. Muscles also play a role in keeping the body warm by contracting and triggering the shiver response – but this is only a short-term fix because prolonged shivering damages muscles. Now it seems that muscles have another way to turn up the heat. "Our findings demonstrate for the first time that muscle, which accounts for 40 per cent of body weight in humans, can generate heat independent of shivering," says Muthu Periasamy of Ohio State University in Columbus. Surviving the chill Through experiments on mice that had their usual thermostat – brown fat – surgically removed, Periasamy and his colleagues proved that a protein called sarcolipin helps muscle cells keep the body warm by burning energy, almost like an idling motor car, even if the muscles do not contract. All of the mice had their brown fat removed, but some of them had been genetically engineered to lack sarcolipin too. These rodents could not survive when held at 4 °C, and died of hypothermia within 10 hours. By contrast, mice that could make sarcolipin were able to survive the chilly temperatures and maintained their core body temperature – despite having no brown fat. © Copyright Reed Business Information Ltd.

Keyword: Obesity; Aggression
Link ID: 17237 - Posted: 09.10.2012

by Colin Barras ON THE face of it, the placebo effect makes no sense. Someone suffering from a low-level infection will recover just as nicely whether they take an active drug or a simple sugar pill. This suggests people are able to heal themselves unaided - so why wait for a sugar pill to prompt recovery? New evidence from a computer model offers a possible evolutionary explanation, and suggests that the immune system has an on-off switch controlled by the mind. It all starts with the observation that something similar to the placebo effect occurs in many animals, says Peter Trimmer, a biologist at the University of Bristol, UK. For instance, Siberian hamsters do little to fight an infection if the lights above their lab cage mimic the short days and long nights of winter. But changing the lighting pattern to give the impression of summer causes them to mount a full immune response. Likewise, those people who think they are taking a drug but are really receiving a placebo can have a response which is twice that of those who receive no pills (Annals of Family Medicine, doi.org/cckm8b). In Siberian hamsters and people, intervention creates a mental cue that kick-starts the immune response. There is a simple explanation, says Trimmer: the immune system is costly to run - so costly that a strong and sustained response could dangerously drain an animal's energy reserves. In other words, as long as the infection is not lethal, it pays to wait for a sign that fighting it will not endanger the animal in other ways. © Copyright Reed Business Information Ltd.

Keyword: Pain & Touch; Aggression
Link ID: 17231 - Posted: 09.07.2012

By Miguel A. L. Nicolelis In 2014 billions of viewers worldwide may remember the opening game of the World Cup in Brazil for more than just the goals scored by the Brazilian national team and the red cards given to its adversary. On that day my laboratory at Duke University, which specializes in developing technologies that allow electrical signals from the brain to control robotic limbs, plans to mark a milestone in overcoming paralysis. If we succeed in meeting still formidable challenges, the first ceremonial kick of the World Cup game may be made by a paralyzed teenager, who, flanked by the two contending soccer teams, will saunter onto the pitch clad in a robotic body suit. This suit—or exoskeleton, as we call it—will envelop the teenager's legs. His or her first steps onto the field will be controlled by motor signals originating in the kicker's brain and transmitted wirelessly to a computer unit the size of a laptop in a backpack carried by our patient. This computer will be responsible for translating electrical brain signals into digital motor commands so that the exoskeleton can first stabilize the kicker's body weight and then induce the robotic legs to begin the back-and-forth coordinated movements of a walk over the manicured grass. Then, on approaching the ball, the kicker will visualize placing a foot in contact with it. Three hundred milliseconds later brain signals will instruct the exoskeleton's robotic foot to hook under the leather sphere, Brazilian style, and boot it aloft. This scientific demonstration of a radically new technology, undertaken with collaborators in Europe and Brazil, will convey to a global audience of billions that brain control of machines has moved from lab demos and futuristic speculation to a new era in which tools capable of bringing mobility to patients incapacitated by injury or disease may become a reality. © 2012 Scientific American

Keyword: Robotics
Link ID: 17220 - Posted: 08.30.2012

Helen Shen Automated assistance may soon be available to neuroscientists tackling the brain’s complex circuitry, according to research presented last week at the Aspen Brain Forum in Colorado. Robots that can find and simultaneously record the activity of dozens of neurons in live animals could help researchers to reveal how connected cells interpret signals from one another and transmit information across brain areas — a task that would be impossible using single-neuron studies. The robots are designed to perform whole-cell patch-clamping, a difficult but powerful method that allows neuroscientists to access neurons' internal electrical workings, says Edward Boyden of the Massachusetts Institute of Technology in Cambridge, who is leading the work. Manually performing the method on live animals requires extensive training to perfect and, as a result, only a handful of neurophysiologists use the technique, says Boyden, who presented at the conference. He is developing the automated tool with Craig Forest at the Georgia Institute of Technology in Atlanta and others. “We think that it helps democratize procedures that require a lot of skill,” he says. In May, the group described how a basic version of the robot can record electrical currents in single neurons in the brains of anaesthetized mice1. The robot finds its target on the basis of characteristic changes in the electrical environment near neurons. Then, the device nicks the cell’s membrane and seals itself around the tiny hole to access the neuron's contents. On 24 August, Boyden presented results showing that a more advanced version of the robot could be used to identify and probe four neurons at once — and he says he wants to push the design further, perhaps to tap as many as 100 neurons at a time. © 2012 Nature Publishing Group

Keyword: Robotics
Link ID: 17215 - Posted: 08.29.2012

By SEAN B. CARROLL Early one evening a few years ago, I took a short hike with my wife, Jamie, in the Cockscomb Basin Wildlife Sanctuary in Belize. The large, lush reserve is known for its healthy population of jaguars, so, following closely behind our guide, we kept our eyes peeled for the elusive cats. We saw a few tracks and some claw marks on trees, but elected to leave the jungle before nightfall. We were very near the end of the trail when we were surprised by a large snake, about six feet long, crossing directly in front of us. Belize has lots of snakes, more than 50 species. Some can get pretty large, like the boa constrictor, which is impressive but harmless. This one was not harmless. Even in the darkening jungle, the triangular pattern on its back allowed me to identify it quickly as a fer-de-lance, the most dangerous snake in Belize. Excited, and comfortable that I was well out of striking range, I reached into my backpack for my video camera and flipped on its “night shot” feature. I now saw the magnificent snake clearly on my LCD screen. As I tried to creep in for a closer shot, however, I felt something holding me back. It was Jamie. She had a grip on my backpack and was concerned that my enthusiasm for snakes had overtaken my judgment. She was not convinced that we were out of range, nor that the snake would not move quickly toward us. I used the zoom and filmed from where I stood. For me to film the snake in the dark, I had to rely on Sony’s innovation and engineering. The camera’s infrared LED source generated light with a longer wavelength than the human eye can detect; those photons then bounced off the snake and were detected by the camera’s infrared sensors and converted into an image. © 2012 The New York Times Company

Keyword: Evolution; Aggression
Link ID: 17210 - Posted: 08.28.2012

By Stephani Sutherland Ice cream headache is a familiar summertime sensation, but the pain's source has been mysterious until now. A team led by Jorge Serrador of Harvard Medical School produced brain scans of “second-by-second changes” in blood flow while subjects sipped iced water through a straw pressed against the roof of the mouth, which caused the brain's major artery to widen. “Blood flow changes actually preceded the pain” that subjects reported, Serrador says. As the vessel narrowed again, the discomfort ebbed. He suspects that the influx of blood is meant to protect the brain from extreme cold and that increased pressure inside the skull could cause the pain. Serrador presented the results at Experimental Biology 2012 in April in San Diego. © 2012 Scientific American

Keyword: Pain & Touch
Link ID: 17205 - Posted: 08.27.2012