Chapter 16. None
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By PAULA SPAN DEDHAM, Mass. — Jerome Medalie keeps his advance directive hanging in a plastic sleeve in his front hall closet, as his retirement community recommends. That’s where the paramedics will look if someone calls 911. Like many such documents, it declares that if he is terminally ill, he declines cardiopulmonary resuscitation, a ventilator and a feeding tube. But Mr. Medalie’s directive also specifies something more unusual: If he develops Alzheimer’s disease or another form of dementia, he refuses “ordinary means of nutrition and hydration.” A retired lawyer with a proclivity for precision, he has listed 10 triggering conditions, including “I cannot recognize my loved ones” and “I cannot articulate coherent thoughts and sentences.” If any three such disabilities persist for several weeks, he wants his health care proxy — his wife, Beth Lowd — to ensure that nobody tries to keep him alive by spoon-feeding or offering him liquids. VSED, short for “voluntarily stopping eating and drinking,” is not unheard-of as an end-of-life strategy, typically used by older adults who hope to hasten their decline from terminal conditions. But now ethicists, lawyers and older adults themselves have begun a quiet debate about whether people who develop dementia can use VSED to end their lives by including such instructions in an advance directive. Experts know of just a handful of people with directives like Mr. Medalie’s. But dementia rates and numbers have begun a steep ascent, already afflicting an estimated 30 percent of those older than 85. Baby boomers are receiving a firsthand view of the disease’s devastation and burdens as they care for aging parents. They may well prove receptive to the idea that they shouldn’t be kept alive if they develop dementia themselves, predicted Alan Meisel, the director of the University of Pittsburgh’s Center for Bioethics and Health Law. © 2015 The New York Times Company
Link ID: 20495 - Posted: 01.20.2015
By Tia Ghose Being around strangers can cause people stress and, in turn, make them less able to feel others' pain, new research suggests. But giving people a drug that blocks the body's stress response can restore that sense of empathy, scientists said. What's more, the same effect shows up in both humans and mice. "In some sense, we've figured out what to do about increasing empathy as a practical matter," said Jeffrey Mogil, a neuroscientist at McGill University in Montreal. "We've figured out what stops it from happening and, therefore, the solution to make it happen more between strangers." Decreasing stress by doing a shared activity could be a simple way to increase empathy between people who don't know each other, the findings suggest. Past studies had found that mice seemed to feel the pain of familiar mice but were less responsive to foreign mice. Other studies found that, in both humans and mice, stress levels tended to rise around strangers. To see how stress and empathy are connected, Mogil and his colleagues placed two mice together in a cage, then inflicted a painful stimulus on one of them. When the mice were cage mates, the unaffected mouse showed more signs of pain than when they were strangers. But when the team gave the mice a drug called metyrapone, which blocks the formation of the stress hormone cortisol, the mice responded equally to the strangers' pain.
Link ID: 20491 - Posted: 01.17.2015
By Viviane Callier In the deep sea, where light is dim and blue, animals with bigger eyes see better—but bigger eyes are more conspicuous to predators. In response, the small (10 mm to 17 mm), transparent crustacean Paraphronima gracilis has evolved a unique eye structure. Researchers collected the animals from 200- to 500-meter deep waters in California’s Monterey Bay using a remote-operated vehicle. They then characterized the pair of compound eyes, discovering that each one was composed of a single row of 12 distinct red retinas. Reporting online on 15 January in Current Biology, the researchers hypothesize that each retina captures an image that is transmitted to the crustacean’s brain, which integrates the 12 images to increase brightness and contrast sensitivity, adapting to changing light levels. Future work will focus on how images are processed by the neural connections between the retinas and the brain. © 2015 American Association for the Advancement of Science.
By Brady Dennis The Food and Drug Administration on Wednesday approved a device aimed at helping obese people shed weight in a novel way – by targeting the nerve pathway between the brain and the stomach that controls feelings of hunger and fullness. The Maestro Rechargeable System, as it is known, consists of an electrical charge generator, wire leads and electrodes that are implanted surgically into a patient’s abdomen. It sends electrical pulses designed to interfere with the vagus nerve, which signals to the brain when the stomach is full or empty. Though researchers don't know exactly how such electrical stimulation leads to weight loss, the approach seems promising. In a year-long clinical trial involving 233 patients with a body-mass index, or BMI, of 35 or greater, those who received a working Maestro device lost 8.5 percent more weight than those without it. About half those in the experimental group lost at least 20 percent of their excess weight, and more than a third lost more than 25 percent of their excess weight. The overall figure was below the original goal of the trial, which was to show weight loss of 10 percent more excess weight in the control group than in those using the new device. Nevertheless, an FDA advisory group said the data showed sustained weight loss among participants and argued that the benefits of the device outweigh its risks for certain patients. In the clinical trial, some patients experienced nausea, vomiting, surgical complications and other side effects. The FDA is requiring the device's manufacturer, EnteroMedics, to conduct a five-year, post-approval study to gather additional data about its safety and effectiveness.
Link ID: 20488 - Posted: 01.15.2015
by Ashley Yeager The brain's got its own set of pipes for flushing waste. The plumbing is delicate, however — a finding that may complicate scientists' attempts to create a blood test to diagnose traumatic brain injuries. Bumps to the head can knock proteins out of brain cells. The brain's plumbing system is supposed to wash these proteins away from the damaged area and eventually into the blood. But new research in mice shows that slight alterations to the brain's self-cleaning system, even from treating head injuries, can change the levels of proteins flushed into the blood. As a result, the proteins are unreliable markers of injury, researchers report January 14 in the Journal of Neuroscience. © Society for Science & the Public 2000 - 2015.
By SAM ROBERTS When he was just 5 years old, Thomas Graboys declared that he intended to become a doctor. As a young physician, he visited a nephew serving in the Peace Corps in Mauritania and remained for two months, treating dozens of patients a day. He skied and played tennis and joined fellow cardiologists as the drummer in a rock band called the Dysrhythmics. In Boston, he was famous as a member of the team that diagnosed the Celtics star Reggie Lewis’s heart defect before he died abruptly on a basketball court. In short, “he was a medical version of one of Tom Wolfe’s masters of the universe,” one reviewer concluded after Dr. Graboys (pronounced GRAY-boys) published his autobiography. But barely 60, after experiencing horrific nightmares, frequently flailing in bed, losing his memory, suffering tremors and finally collapsing on his wedding day, he acknowledged that he was suffering from Parkinson’s disease and the onset of dementia. He informed his patients that he had no choice but to close his practice. “My face is often expressionless, though I still look younger than my 63 years,” he recalled in the autobiography, “Life in the Balance: A Physician’s Memoir of Life, Love, and Loss With Parkinson’s Disease and Dementia,” which was published in 2008. “I am stooped,” he continued. “I shuffle when I walk, and my body trembles. My train of thought regularly runs off the rails. There is no sugarcoating Parkinson’s. There is no silver lining here. There is anger, pain, and frustration at being victimized by a disease that can to some extent be managed but cannot be cured.” After managing for more than a decade, Dr. Graboys died on Jan. 5 at his home in Chestnut Hill, Mass., his daughter, Penelope Graboys Blair, said. The cause was complications of Lewy Body Dementia, which was diagnosed after his Parkinson’s. He was 70. © 2015 The New York Times Company
Link ID: 20485 - Posted: 01.15.2015
By Will Boggs MD NEW YORK (Reuters Health) - Patients with chronic pain show signs of glial activation in brain centers that modulate pain, according to results from a PET-MRI study. "Glia appears to be involved in the pathophysiology of chronic pain, and therefore we should consider developing therapeutic approaches targeting glia," Dr. Marco L. Loggia from Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, told Reuters Health by email. "Glial activation is accompanied by many cellular responses, which include the production and release of substances (such as so-called 'pro-inflammatory cytokines') that can sensitize the pain pathways in the central nervous system," he explained. "Thus, glial activation is not a mere reaction to a pain state but actively contributes to the establishment and/or maintenance of persistent pain." To test their hypothesis that patients with chronic pain demonstrate in vivo activation of brain glia, Dr. Loggia's team imaged the brains of 19 individuals diagnosed with chronic low back pain as well as 25 pain-free healthy volunteers using 11C-PBR28, a PET radioligand that binds to the translocator protein (TSPO), a protein upregulated in activated microglia and reactive astrocytes in animal models of pain. Each patient exhibited higher 11C-PBR28 uptakes than his/her age-, sex-, and TSPO genotype-matched control in the thalamus, and there were no brain regions for which the healthy controls showed statistically higher uptakes than the patients with chronic low back pain. © 2015 Scientific American
By Michael Balter If there’s one thing that distinguishes humans from other animals, it’s our ability to use language. But when and why did this trait evolve? A new study concludes that the art of conversation may have arisen early in human evolution, because it made it easier for our ancestors to teach each other how to make stone tools—a skill that was crucial for the spectacular success of our lineage. Researchers have long debated when humans starting talking to each other. Estimates range wildly, from as late as 50,000 years ago to as early as the beginning of the human genus more than 2 million years ago. But words leave no traces in the archaeological record. So researchers have used proxy indicators for symbolic abilities, such as early art or sophisticated toolmaking skills. Yet these indirect approaches have failed to resolve arguments about language origins. Now, a team led by Thomas Morgan, a psychologist at the University of California, Berkeley, has attacked the problem in a very different way. Rather than considering toolmaking as a proxy for language ability, he and his colleagues explored the way that language may helps modern humans learn to make such tools. The researchers recruited 184 students from the University of St. Andrews in the United Kingdom, where some members of the team were based, and organized them into five groups. The first person in each group was taught by archaeologists how to make artifacts called Oldowan tools, which include fairly simple stone flakes that were manufactured by early humans beginning about 2.5 million years ago. This technology, named after the famous Olduvai Gorge in Tanzania where archaeologists Louis and Mary Leakey discovered the implements in the 1930s, consists of hitting a stone “core” with a stone “hammer” in such a way that a flake sharp enough to butcher an animal is struck off. Producing a useful flake requires hitting the core at just the right place and angle. © 2015 American Association for the Advancement of Science.
By Susan Svrluga Edwin Chapman’s secretary handed him a pile of prescription slips, and the doctor’s pen moved quickly across them: “Buprenorphine/naloxone.” “Buprenorphine/naloxone.” “Buprenorphine/naloxone.” His waiting room was full of heroin-addicted patients there to refill their generic prescriptions for Suboxone, a drug that helps keep their relentless cravings at bay and now outpaces methadone as a treatment. Chapman is an internist, a cardiologist. This drug has transformed his D.C. medical practice — now more than half of his patients are there to seek it, addicts edging out elderly ladies with arthritis and diabetes. And the drug, he believes, has transformed lives. He wishes more people could get it. Yet even as heroin use surges in the United States, destroying neighborhoods and families — drug overdoses kill more people than any other kind of accident — both addicts and doctors say there are barriers that keep some from the treatment they desperately need. “In the past we’ve kind of run away from these patients, put them in methadone clinics, places no one can see them,” said Chapman, who estimates that two-thirds of his heroin-addicted patients tested positive for hepatitis C and more than one in 10 for HIV. “We need to reverse that. Put them in primary care. We need to be taking care of sick folks, not running away from them.
Keyword: Drug Abuse
Link ID: 20480 - Posted: 01.14.2015
By Neuroskeptic A new study offers two reasons to be cautious about some of the claims made for the role of the hormone oxytocin in human behavior. The paper’s out now in PLoS ONE from researchers James C. Christensen and colleagues, who are based at the US Air Force Research Laboratory in Ohio. That the military are interested in oxytocin at all is perhaps a testament to the huge amount of interest that this molecule has attracted in recent years. Oxytocin has been called the “hug hormone”, and is said to be involved in such nice things as love and trust. But according to Christensen et al., quite a lot of previous oxytocin research may be flawed. Their paper is in two parts. Christensen et al. first show that the only accurate way to measure oxytocin levels in blood is by performing plasma extraction before chemical analysis. Using unextracted plasma, they find, leads to seriously distorted measures. The differences between extracted and unextracted plasma estimates of oxytocin have been noted before, but Christensen et al. show directly that unextracted plasma interferes with oxytocin measurement. They found that oxytocin test kits were unable to detect a ‘spike’ of pure oxytocin added to some unextracted plasma samples, whereas the spike was reliably detected when added to an extracted sample. This was true using either the ELISA or RIA method for quantification of oxytocin. With ELISA, unextracted oxytocin measures were also very noisy and unrealistically high:
Keyword: Hormones & Behavior
Link ID: 20479 - Posted: 01.14.2015
Vernon Mountcastle, one of Johns Hopkins Medicine's giants of the 20th century, died peacefully at his North Baltimore home on Sunday, with Nancy, his wife of seven decades, and family at his bedside. He was 96. Mountcastle was universally acknowledged as the "father of neuroscience" and served Johns Hopkins with extraordinary dedication for nearly 65 years. A 1942 graduate of the School of Medicine and a member of the faculty since 1948, Mountcastle served as director of the Department of Physiology and head of the Philip Bard Laboratories of Neurophysiology at Johns Hopkins from 1964 to 1980. He later became one of the founding members of Johns Hopkins' Zanvyl Krieger Mind/Brain Institute, where he continued to work until his retirement at 87. Colleagues remember his dedication to the professional development of neuroscientists, fiercely focused work ethic, and devotion to collaborative research. Also see: Mind/Brain's Mountcastle wins NAS award for lifetime of groundbreaking work (Gazette, April 1998) Mountcastle once was dubbed the "Jacques Cousteau of the cortex" for his revolutionary research delving into the unknown depths of the brain and establishing the basis for modern neuroscience. In 1957, he made the breakthrough discovery that revolutionized the concept of how the brain is built. He found that the cells of the cerebral cortex are organized in vertical columns, extending from the surface of the brain down through six layers of the cortex, each column processing a specific kind of information.
Keyword: Brain imaging
Link ID: 20478 - Posted: 01.14.2015
By CATHERINE SAINT LOUIS A nationwide outbreak of a respiratory virus last fall sent droves of children to emergency departments. The infections have now subsided, as researchers knew they would, but they have left behind a frightening mystery. Since August, 103 children in 34 states have had an unexplained, poliolike paralysis of an arm or leg. Each week, roughly three new cases of so-called acute flaccid myelitis are still reported to the Centers for Disease Control and Prevention. Is the virus, called enterovirus 68, really the culprit? Experts aren’t certain: Unexplained cases of paralysis in children happen every year, but they are usually scattered and unrelated. After unusual clusters of A.F.M. appeared this fall, enterovirus 68 became the leading suspect, and now teams of researchers are racing to figure out how it could have led to such damage. “It’s unsatisfying to have an illness and not know what caused it,” said Dr. Samuel Dominguez, an epidemiologist and an infectious disease specialist at Children’s Hospital Colorado, which has had the largest cluster of patients. For many families, the onset of persistent limb paralysis has been a bewildering experience. Roughly two thirds of the children with A.F.M. have reported some improvement, according to the C.D.C. About a third show none. Only one child has fully recovered. In August, Jack Wernick, a first grader in Kingsport, Tenn., developed a “crummy little cold,” said his father, Dan Wernick, who works for a paper company. It seemed ordinary, until Jack complained that his right arm was heavy, his face began drooping and pain started shooting down his right leg. © 2015 The New York Times Company
Keyword: Movement Disorders
Link ID: 20477 - Posted: 01.13.2015
by Clare Wilson Could a lopsided gap help set us apart from our primate cousins? Our brains and chimps' are built differently in the areas that give us our social skills and language. The human brain has a 4.5-centimetre-long groove running deeper along the right side than the left. Chimp brains lack this asymmetry, as François Leroy of the French National Institute of Health and Medical Research in Saclay, and colleagues, have discovered. The groove's function is unknown, but its location suggests it played a role in the evolution of our communication abilities. "One day this will help us understand what makes us tick," says Colin Renfrew of the University of Cambridge, who was not involved in the study. Although our brain is about three times the size of a chimp's, anatomical features that only the human brain possesses are surprisingly hard to find. One known difference is in a region called Broca's area, which is also involved in speech and is larger in humans than chimps. The asymmetrical groove in humans was also known, but the new study, in which 177 people and 73 chimps had brain scans, revealed it is almost completely absent in the other primates. In humans, the deeper groove in the right brain lies in the region that controls voice and face recognition and working out what other people are thinking – our so-called theory of mind. The shallower groove on the left is at the heart of the areas associated with language. The lack of symmetry could signify that tissue layers in the right brain have been reorganised, says Leroy. © Copyright Reed Business Information Ltd.
By KIRA PEIKOFF At a recent Seahawks football game in Seattle, Shy Sadis, 41, took a drag on a slim vapor pen that looked like a jet black Marlboro. The tip glowed red as he inhaled. But the pen contained no nicotine. Instead, it held 250 milligrams of cannabis oil loaded with THC, the psychoactive ingredient in marijuana. “Nobody noticed,” said Mr. Sadis, who owns several marijuana dispensaries in Washington State. “You pull it out of your pocket, take a hit like a cigarette, put it back, and you’re done. It’s so discreet.” The device, called a JuJu Joint, heralds a union that seems all but inevitable: marijuana and the e-cigarette, together at last in an e-joint. For years, people have been stuffing marijuana in various forms into portable vaporizers and into the cartridges of e-cigarettes. But the JuJu Joint is disposable, requires no charging of batteries or loading of cartridges, and comes filled with 150 hits. You take it out of the package and put it to your lips — that’s it. There is no smoke and no smell. Since their introduction in April, 75,000 JuJu Joints have been sold in Washington State, where marijuana is recreationally and medically legal. The maker says that 500,000 will be sold this year and that there are plans to expand to Colorado and Oregon, where recreational use is legal, and to Nevada, where it is decriminalized. “I wanted to eliminate every hassle that has to do with smoking marijuana,” said Rick Stevens, 62, the inventor and co-founder of JuJu Joints with Marcus Charles, a Seattle entrepreneur. “I wanted it to be discreet and easy for people to handle. There’s no odor, matches or mess.” © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 20473 - Posted: 01.13.2015
By GARETH COOK In 2005, Sebastian Seung suffered the academic equivalent of an existential crisis. More than a decade earlier, with a Ph.D. in theoretical physics from Harvard, Seung made a dramatic career switch into neuroscience, a gamble that seemed to be paying off. He had earned tenure from the Massachusetts Institute of Technology a year faster than the norm and was immediately named a full professor, an unusual move that reflected the sense that Seung was something of a superstar. His lab was underwritten with generous funding by the elite Howard Hughes Medical Institute. He was a popular teacher who traveled the world — Zurich; Seoul, South Korea; Palo Alto, Calif. — delivering lectures on his mathematical theories of how neurons might be wired together to form the engines of thought. And yet Seung, a man so naturally exuberant that he was known for staging ad hoc dance performances with Harvard Square’s street musicians, was growing increasingly depressed. He and his colleagues spent their days arguing over how the brain might function, but science offered no way to scan it for the answers. “It seemed like decades could go by,” Seung told me recently, “and you would never know one way or another whether any of the theories were correct.” That November, Seung sought the advice of David Tank, a mentor he met at Bell Laboratories who was attending the annual meeting of the Society for Neuroscience, in Washington. Over lunch in the dowdy dining room of a nearby hotel, Tank advised a radical cure. A former colleague in Heidelberg, Germany, had just built a device that imaged brain tissue with enough resolution to make out the connections between individual neurons. But drawing even a tiny wiring diagram required herculean efforts, as people traced the course of neurons through thousands of blurry black-and-white images. What the field needed, Tank said, was a computer program that could trace them automatically — a way to map the brain’s connections by the millions, opening a new area of scientific discovery. For Seung to tackle the problem, though, it would mean abandoning the work that had propelled him to the top of his discipline in favor of a highly speculative engineering project. © 2015 The New York Times Company
Keyword: Brain imaging
Link ID: 20470 - Posted: 01.10.2015
by Michael Hotchkiss Forget about it. Your brain is a memory powerhouse, constantly recording experiences in long-term memory. Those memories help you find your way through the world: Who works the counter each morning at your favorite coffee shop? How do you turn on the headlights of your car? What color is your best friend's house? But then your barista leaves for law school, you finally buy a new car and your buddy spends the summer with a paint brush in hand. Suddenly, your memories are out of date. What happens next? An experiment conducted by researchers from Princeton University and the University of Texas-Austin shows that the human brain uses memories to make predictions about what it expects to find in familiar contexts. When those subconscious predictions are shown to be wrong, the related memories are weakened and are more likely to be forgotten. And the greater the error, the more likely you are to forget the memory. "This has the benefit ultimately of reducing or eliminating noisy or inaccurate memories and prioritizing those things that are more reliable and that are more accurate in terms of the current state of the world," said Nicholas Turk-Browne, an associate professor of psychology at Princeton and one of the researchers. The research was featured in an article, "Pruning of memories by context-based prediction error," that appeared in 2014 in the Proceedings of the National Academy of Sciences. The other co-authors are Ghootae Kim, a Princeton graduate student; Jarrod Lewis-Peacock, an assistant professor of psychology at the University of Texas-Austin; and Kenneth Norman, a Princeton professor of psychology and the Princeton Neuroscience Institute. © Medical Xpress 2011-2014,
Keyword: Learning & Memory
Link ID: 20469 - Posted: 01.10.2015
By Richard A. Friedman, M.D. You’re feeling down, and your doctor or therapist has confirmed it: You have depression. Now what? Until recently, many experts thought that your clinician could literally pick any antidepressant or type of psychotherapy at random because, with a few clinical exceptions, there was little evidence to favor one treatment over another for a given patient. In fact, I used to delight in tormenting the drug company representatives when they asked me how I picked an antidepressant. I would take a quarter out of my pocket, flip the coin and say I’d let chance decide because their drug was no better or worse than their competitors’. Although the holy grail of personalized therapy — be it with psychotropic drugs or psychotherapy — has proved elusive, we’ve learned a lot recently about individual factors that might predict a better response to one type of treatment over another. Dr. Helen Mayberg, a professor of psychiatry at Emory University, recently published a study in JAMA Psychiatry that identified a potential biomarker in the brain that could predict whether a depressed patient would respond better to psychotherapy or antidepressant medication. Using PET scans, she randomized a group of depressed patients to either 12 weeks of treatment with the S.S.R.I. antidepressant Lexapro or to cognitive behavior therapy, which teaches patients to correct their negative and distorted thinking. Over all, about 40 percent of the depressed subjects responded to either treatment. But Dr. Mayberg found striking brain differences between patients who did well with Lexapro compared with cognitive behavior therapy, and vice versa. Patients who had low activity in a brain region called the anterior insula measured before treatment responded quite well to C.B.T. but poorly to Lexapro; conversely, those with high activity in this region had an excellent response to Lexapro, but did poorly with C.B.T. © 2015 The New York Times Company
Link ID: 20468 - Posted: 01.10.2015
Ewen Callaway The ability to recognize oneself in a mirror has been touted as a hallmark of higher cognition — present in humans and only the most intelligent of animals — and the basis for empathy. A study published this week in Current Biology controversially reports that macaques can be trained to pay attention to themselves in a mirror, the first such observation in any monkey species1. Yet the finding raises as many questions as it answers — not only about the cognitive capacity of monkeys, but also about mirror self-recognition as a measure of animal intelligence. “Simply because you’re acting as if you recognize yourself in a mirror doesn’t necessarily mean you’ve achieved self-recognition,” says Gordon Gallup, an evolutionary psychologist at the State University of New York in Albany, who in 1970 was the first to demonstrate mirror self-recognition in captive chimpanzees2. When most animals encounter their reflections in a mirror, they act as if they have seen another creature. They lash out aggressively, belt out loud calls and display other social behaviours. This is how chimps first acted when Gallup placed a full-length mirror next to their cages. But after a couple of days, their attitudes changed and they started examining themselves, says Gallup. “They’d look at the inside of their mouths; they’d watch their tongue move.” This convinced him that the chimps recognized themselves in the mirror. He knew other scientists would be sceptical, so he developed a test of mirror self-recognition. After chimps started acting as if they saw themselves in the mirror, after about 10 days, he anaesthetized them and applied an odour-free red mark to a location on their faces they could not see, such as above the brow ridge. © 2015 Nature Publishing Group
Link ID: 20467 - Posted: 01.10.2015
By ANDREW POLLACK Driving to a meeting in 2008, Jay Lichter, a venture capitalist, suddenly became so dizzy he had to pull over and call a friend to take him to the emergency room. The diagnosis: Ménière’s disease, a disorder of the inner ear characterized by debilitating vertigo, hearing loss and tinnitus, or ringing in the ears. But from adversity can spring opportunity. When Mr. Lichter learned there were no drugs approved to treat Ménière’s, tinnitus or hearing loss, he started a company, Otonomy. It is one of a growing cadre of start-ups pursuing drugs for the ear, an organ once largely neglected by the pharmaceutical industry. Two such companies, Otonomy and Auris Medical, went public in 2014. Big pharmaceutical companies like Pfizer and Roche are also exploring the new frontier. A clinical trial recently began of a gene therapy being developed by Novartis that is aimed at restoring lost hearing. The sudden flurry of activity has not yet produced a drug that improves hearing or silences ringing in the ears, but some companies are reporting hints of promise in early clinical trials. There is a huge need, some experts say. About 48 million Americans have a meaningful hearing loss in at least one ear; 30 million of them have it in both ears, said Dr. Frank R. Lin, an associate professor of otolaryngology and geriatric medicine at Johns Hopkins University. That figure is expected to increase as baby boomers grow older. © 2015 The New York Times Company
Link ID: 20466 - Posted: 01.10.2015
By James Gallagher Health editor, BBC News website An elastic implant that moves with the spinal cord can restore the ability to walk in paralysed rats, say scientists. Implants are an exciting field of research in spinal cord injury, but rigid designs damage surrounding tissue and ultimately fail. A team at Ecole Polytechnique Federale de Lausanne (EPFL) has developed flexible implants that work for months. It was described by experts as a "groundbreaking achievement of technology". The spinal cord is like a motorway with electrical signals rushing up and down it instead of cars. Injury to the spinal cord leads to paralysis when the electrical signals are stuck in a jam and can no longer get from the brain to the legs. The same group of researchers showed that chemically and electrically stimulating the spinal cord after injury meant rats could "sprint over ground, climb stairs and even pass obstacles". Rat walks up stairs Previous work by the same researchers But that required wired electrodes going directly to the spinal cord and was not a long-term option. Implants are the next step, but if they are inflexible they will rub, causing inflammation, and will not work properly. The latest innovation, described in the journal Science, is an implant that moves with the body and provides both chemical and electrical stimulation. When it was tested on paralysed rats, they moved again. One of the scientists, Prof Stephanie Lacour, told the BBC: "The implant is soft but also fully elastic to accommodate the movement of the nervous system. "The brain pulsates with blood so it moves a lot, the spinal cord expands and retracts many times a day, think about bending over to tie your shoelaces. "In terms of using the implant in people, it's not going to be tomorrow, we've developed dedicated materials which need approval, which will take time. © 2015 BBC.
Link ID: 20465 - Posted: 01.10.2015