Chapter 11. Motor Control and Plasticity

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Catherine Offord The Japanese government’s health ministry has given the go-ahead for a trial of human induced pluripotent stem cells to treat spinal cord injury, Reuters reports today (February 18). Researchers at Keio University plan to recruit four adults who have sustained recent nerve damage in sports or traffic accidents. “It’s been 20 years since I started researching cell treatment. Finally we can start a clinical trial,” Hideyuki Okano of Keio University School of Medicine told a press conference earlier today, The Japan Times reports. “We want to do our best to establish safety and provide the treatment to patients.” The team’s intervention involves removing differentiated cells from patients and reprogramming them via human induced pluripotent stem cells (iPSCs) into neural cells. Clinicians will then inject about 2 million of these cells into each patient’s site of injury. The approach has been successfully tested in a monkey, which recovered the ability to walk after paralysis, according to the Times. It’s not the first time Japan has approved the use of iPSCs in clinical trials. Last year, researchers at Kyoto University launched a trial using the cells to treat Parkinson’s disease. And in 2014, a team at the RIKEN Center for Developmental Biology led the first transplant of retina cells grown from iPSCs to treat a patient’s eye disease. © 1986 - 2019 The Scientist

Keyword: Regeneration; Stem Cells
Link ID: 25976 - Posted: 02.21.2019

By Gretchen Reynolds Exercise and eating have a fraught, unsettled relationship with each other. Workouts can blunt or boost appetites. People who start an exercise program often overeat and gain weight — and yet studies and lived experience demonstrate that regular exercise is needed to avoid regaining the weight lost during a successful diet. Intrigued by these contradictory outcomes, researchers at the University of Texas Southwestern Medical Center, along with colleagues from other institutions, ran an experiment on the melanocortin circuit, a brain network in the hypothalamus known to be involved in metabolism. The resulting study, published in December in Molecular Metabolism, suggests that intense exercise might change the workings of certain neurons in ways that could have beneficial effects on appetite and metabolism. The melanocortin circuit consists mainly of two types of neurons. The neuropeptide Y (NPY) cells relay signals encouraging the body to seek food, while the pro-opiomelanocortin (POMC) neurons countermand those orders, reducing interest in food. Animals, including humans, that lack healthy POMC neurons usually become morbidly obese. The researchers focused on what exercise would do to these cells in mice, whose melanocortin circuits resemble ours. Healthy adult male mice either ran on small treadmills or, in a control group, were placed on unmoving treadmills. The exercise routine consisted of 60 minutes of fast, intense running, broken into three 20-minute blocks. Afterward, the mice were free to eat or not, as they chose. The researchers then checked neuronal activity in some of their brains by microscopically probing individual cells in living tissue to measure their electrical and biochemical signals. The tests were repeated throughout the study, which ran for as many as 10 days for some mice. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 25911 - Posted: 01.29.2019

David Cyranoski Japan has approved a stem-cell treatment for spinal-cord injuries. The event marks the first such therapy for this kind of injury to receive government approval for sale to patients. “This is an unprecedented revolution of science and medicine, which will open a new era of healthcare,” says oncologist Masanori Fukushima, head of the Translational Research Informatics Center, a Japanese government organization in Kobe that has been giving advice and support to the project for more than a decade. But independent researchers warn that the approval is premature. Ten specialists in stem-cell science or spinal-cord injuries, who were approached for comment by Nature and were not involved in the work or its commercialization, say that evidence that the treatment works is insufficient. Many of them say that the approval for the therapy, which is injected intravenously, was based on a small, poorly designed clinical trial. They say that the trial’s flaws — including that it was not double-blinded — make it difficult to assess the treatment’s long-term efficacy, because it is hard to rule out whether patients might have recovered naturally. And, although the cells used — known as mesenchymal stem cells (MSCs) — are thought to be safe, the infusion of stem cells into the blood has been connected with dangerous blood clots in the lungs. And all medical procedures carry risks, which makes them hard to justify unless they are proven to offer a benefit. © 2019 Springer Nature Publishing AG

Keyword: Regeneration; Stem Cells
Link ID: 25896 - Posted: 01.24.2019

By David Blum Many of us have personally experienced or witnessed the impact of Parkinson’s disease (PD), a movement disorder that affects nearly 10 million people worldwide. This chronic, progressive neurodegenerative disorder leads to disability from motor impairments, such as tremors, rigidity, absence or slowness of movement and impaired balance, as well as from non-motor symptoms including sleep disruption, gastrointestinal issues, sexual dysfunction or loss of sense of smell or taste, to name a few. The ideal outcome of PD clinical research would be to find a cure. But researchers are also looking at novel ways to administer proven Parkinson’s medicines in order to help people living with the disease better control their symptoms and maintain their regular, daily activities. The brain cells that die from PD are responsible for producing dopamine, a neurotransmitter involved in complex behaviors including motor coordination, addiction and motivation. As a result, treatment typically includes the use of levodopa—a medication that is converted into dopamine in the brain and relieves PD symptoms. For the first few years after diagnosis, many individuals’ symptoms are well controlled by levodopa. The average age of onset is 60, but some people are diagnosed at 40 or even younger, potentially requiring treatment for decades. Over time, a patient’s response to levodopa changes, and the therapeutic window, or period when levodopa is effective, narrows, often leading to the prescription of additional levodopa or more frequent dosing of levodopa to manage symptoms. © 2019 Scientific American

Keyword: Parkinsons
Link ID: 25883 - Posted: 01.19.2019

By Elie Dolgin The compound eyes of the common fruit fly are normally brick red. But in neurologist Tom Lloyd's lab at Johns Hopkins University School of Medicine in Baltimore, Maryland, many of the fly eyes are pocked with white and black specks, a sign that neurons in each of their 800-odd eye units are shriveling away and dying. Those flies have the genetic equivalent of amyotrophic lateral sclerosis (ALS), the debilitating neurodegenerative disorder also known as Lou Gehrig's disease, and their eyes offer a window into the soul of the disease process. By measuring the extent of damage to each insect's eyes, researchers can quickly gauge whether a drug, genetic modification, or some other therapeutic intervention helps stop neuronal loss. Those eyes have also offered an answer to the central mystery of ALS: just what kills neurons—and, ultimately, the patient. The flies carry a mutation found in about 40% of ALS patients who have a family history of the disease, and in about 10% of sporadic cases. The mutation, in a gene called C9orf72, consists of hundreds or thousands of extra copies of a short DNA sequence, just six bases long. They lead to unusually large strands of RNA that glom onto hundreds of proteins in the cell nucleus, putting them out of action. Some of those RNA-ensnared proteins, Lloyd and his Hopkins colleague Jeffrey Rothstein hypothesized, might hold the key to ALS. © 2018 American Association for the Advancement of Science

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25874 - Posted: 01.17.2019

By Laura Spinney A disease mystery with no shortage of leads now has an intriguing new one. Since the 1960s, thousands of children in poor, war-torn regions of East Africa have developed epilepsy-like seizures in which their heads bob to their chest; over time, the seizures worsen, cognitive problems develop, and the victims ultimately die. Researchers have proposed causes for nodding syndrome that include malnutrition, parasites, and viruses, but have not proved a clear link to any of them. Now, the first published examination of the brains of children who died after developing the condition suggests it has a key similarity to certain brain diseases of old age, such as Alzheimer's and Parkinson's: It leaves victims' brains riddled with fibrous tangles containing a protein called tau. "Nodding syndrome is a tauopathy," concludes Michael Pollanen, a pathologist at the University of Toronto in Canada who is lead author of a report published last month in Acta Neuropathologica. Pollanen believes the finding "suggests a totally new line of investigation" into the syndrome. As significant as the discovery of the tangles may be what his group of Canadian and Ugandan researchers didn't find: any sign of the brain inflammation that might be triggered by a parasite or virus. "Our hypothesis is that nodding syndrome is a neurodegenerative disease, like Alzheimer's," Pollanen says. Some who study the condition are skeptical, but the possibility excites researchers working on other tauopathies including Alzheimer's. Childhood forms of those diseases are exceedingly rare, but the nodding syndrome finding "means [tau deposition] is not an age-dependent problem," says John Hardy, of the UK Dementia Research Institute at University College London. Something else must have triggered the tauopathy in these children. And because nodding syndrome struck a small region of East Africa, over a specific time period—in Uganda, the condition appears to be vanishing—its trigger might be relatively easy to identify, and could shed light on the causes of diseases like Alzheimer's, Hardy and others say. © 2018 American Association for the Advancement of Science.

Keyword: Alzheimers; Parkinsons
Link ID: 25805 - Posted: 12.20.2018

Laura Sanders An Alzheimer’s protein found in contaminated vials of human growth hormone can spread in the brains of mice. That finding, published online December 13 in Nature, adds heft to the idea that, in very rare cases, amyloid-beta can travel from one person’s brain to another’s. Decades ago, over a thousand young people in the United Kingdom received injections of growth hormone derived from cadavers’ brains as treatment for growth deficiencies. Four of these people died with unusually high levels of A-beta in their brains, a sign of Alzheimer’s disease (SN: 10/17/15, p. 12). The results hinted that A-beta may have been delivered along with the growth hormone. Now researchers have confirmed not only that A-beta was in some of those old vials, but also that it can spark A-beta accumulation in mice’s brains. Neurologist John Collinge of University College London and colleagues found that brain injections of the contaminated growth hormone led to clumps of A-beta in the brains of mice genetically engineered to produce the protein, while brain injections with synthetic growth hormone did not. The results suggest that A-beta can “seed” the protein in people’s brains, under the right circumstances. Still, that doesn’t mean that Alzheimer’s disease is transmissible in day-to-day life. |© Society for Science & the Public 2000 - 2018

Keyword: Alzheimers; Prions
Link ID: 25788 - Posted: 12.15.2018

Tom Goldman Tim Green first noticed the symptoms about five years ago. The former NFL player, whose strength was a job requirement, suddenly found his hands weren't strong enough to use a nail clipper. His words didn't come out as fast as he was thinking them. "I'm a strange guy," Tim says. "I get something in my head and I can just run with it. I was really afraid I had ALS. But there was enough doubt that I said, 'Alright, I don't. Let's not talk about it. Let's not do anything.' " Denying pain and injury had been a survival strategy in football. "I was well trained in that verse," he says. But a diagnosis in 2016 made denial impossible. Doctors confirmed that Tim, also a former NPR commentator, had ALS, known as Lou Gehrig's disease. The degenerative illness attacks the body's motor nerve cells, weakening muscles in the arms and legs as well as the muscles that control speech, swallowing and breathing. Tim tried to keep it private — he didn't want people feeling sorry for him. But he says, "I got to a point where I couldn't hide it anymore." So Tim went on 60 Minutes and revealed his illness. "What we said is, you either write your own history or someone's going to write it for you," says his 24-year-old son, Troy Green. When one isn't enough I was one of Tim Green's producers for his Morning Edition commentaries back in the 1990s. We went to dinner once when he was in Washington, D.C., for a game — his Atlanta Falcons were playing Washington. Tim had a huge plate of pasta. When we finished, the waiter came over and asked, "Anything else?" Tim pointed to his clean plate and said, "Yeah. Let's do it again." © 2018 npr

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25785 - Posted: 12.13.2018

Laura Beil Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons. Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old. Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find. With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain. “I had an initial hunch that food and food quality was part of the issue,” she says. If something in the environment triggered Parkinson’s, as some theories suggest, it made sense to her that the disease would involve the digestive system. Every time we eat and drink, our insides encounter the outside world. |© Society for Science & the Public 2000 - 2018.

Keyword: Parkinsons; Neuroimmunology
Link ID: 25765 - Posted: 12.08.2018

Sara Reardon Infectious-disease researchers hunting for the cause of a mysterious illness that is paralysing children are combining machine learning with a new gene-sequencing technique to pin down the culprit. The disease, called acute flaccid myelitis (AFM), causes limb weakness and paralysis that resembles the symptoms of polio. The US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, has confirmed 134 cases of AFM in the United States so far this year. Many of those who develop the illness never recover. Most of the evidence suggests that an enterovirus called EV-D681 is causing the illness, but researchers haven’t been able to find the pathogen in the spinal fluid of sick children. Scientists are trying to identify the culprit by using a combination of host-response diagnostics — which look at how the immune system responds to pathogens — and machine-learning analysis. The approach could lead to better diagnostics and provide hints about new treatments. Host-response diagnostic tests haven’t been used in the clinic yet. But researchers are developing similar tests to help pinpoint other conditions that can be tricky to diagnose, including tuberculosis and bacterial meningitis. This year’s AFM outbreak started in October, and is the third in a series of outbreaks in the United States that began in 2014. They have occurred every other year since, though researchers have yet to find a definitive explanation for the pattern. It is also taking scientists an unusually long time to determine the cause of the illness, says William Weldon, a microbiologist at the CDC. © 2018 Springer Nature Publishing AG

Keyword: Movement Disorders; Neuroimmunology
Link ID: 25758 - Posted: 12.07.2018

Robin McKie Science Editor Lawyers are bringing a case against a London hospital trust that could trigger major changes to the rules governing patient confidentiality. The case involves a woman who is suing doctors because they failed to tell her about her father’s fatal hereditary disease before she had her own child. The woman discovered – after giving birth – that her father carried the gene for Huntington’s disease, a degenerative, incurable brain condition. Later she found out she had inherited the gene and that her own daughter, now eight, has a 50% chance of having it. The woman – who cannot be named for legal reasons – says she would have had an abortion had she known about her father’s condition, and is suing the doctors who failed to tell her about the risks she and her child faced. It is the first case in English law to deal with a relative’s claim over issues of genetic responsibility. “This could really change the way we do medicine, because it is about the duty that doctors have to share genetic test results with relatives and whether the duty exists in law,” said Anna Middleton, head of society and ethics research at the Wellcome Genome Campus in Cambridge. Experts say that as more is discovered about the genetic components of medical conditions, including cancer and dementia, doctors will come under increasing pressure to consider not only their patients’ needs but also those of relatives who may share affected genes. The case also raises questions over how much effort clinicians need to put into tracing relatives, and whether they will be sued if their attempts do not go far enough. © 2018 Guardian News and Media Limited

Keyword: Huntingtons
Link ID: 25720 - Posted: 11.26.2018

Ashley Yeager For an hour a day, five days a week, mice in Hiroshi Maejima’s physiology lab at Hokkaido University in Sapporo, Japan, hit the treadmill. The researcher’s goal in having the animals follow the exercise routine isn’t to measure their muscle mass or endurance. He wants to know how exercise affects their brains. Researchers have long recognized that exercise sharpens certain cognitive skills. Indeed, Maejima and his colleagues have found that regular physical activity improves mice’s ability to distinguish new objects from ones they’ve seen before. Over the past 20 years, researchers have begun to get at the root of these benefits, with studies pointing to increases in the volume of the hippocampus, development of new neurons, and infiltration of blood vessels into the brain. Now, Maejima and others are starting to home in on the epigenetic mechanisms that drive the neurological changes brought on by physical activity. In October, Maejima’s team reported that the brains of rodents that ran had greater than normal histone acetylation in the hippocampus, the brain region considered the seat of learning and memory.1 The epigenetic marks resulted in higher expression of Bdnf, the gene for brain-derived neurotrophic factor (BDNF). By supporting the growth and maturation of new nerve cells, BDNF is thought to promote brain health, and higher levels of it correlate with improved cognitive performance in mice and humans. With a wealth of data on the benefits of working out emerging from animal and human studies, clinicians have begun prescribing exercise to patients with neurodegenerative diseases such as Parkinson’s and Alzheimer’s, as well as to people with other brain disorders, from epilepsy to anxiety. Many clinical trials of exercise interventions for neurodegenerative diseases, depression, and even aging are underway. Promising results could bolster the use of exercise as a neurotherapy. © 1986 - 2018 The Scientist

Keyword: Learning & Memory; Muscles
Link ID: 25713 - Posted: 11.24.2018

National Institutes of Health scientists and their colleagues have found evidence of the infectious agent of sporadic Creutzfeldt-Jakob disease (CJD) in the eyes of deceased CJD patients. The finding suggests that the eye may be a source for early CJD diagnosis and raises questions about the safety of routine eye exams and corneal transplants. Sporadic CJD, a fatal neurodegenerative prion disease of humans, is untreatable and difficult to diagnose. Prion diseases originate when normally harmless prion protein molecules become abnormal and gather in clusters and filaments in the body and brain. Scientists hope that early diagnosis of prion and related diseases—such as Alzheimer’s, Parkinson’s and dementia with Lewy bodies—could lead to effective treatments that slow or prevent these diseases. Scientists from NIH’s National Institute of Allergy and Infectious Diseases (NIAID) collaborated on the research with colleagues from the University of California at San Diego and UC-San Francisco. About 40 percent of sporadic CJD patients develop eye problems that could lead to an eye exam, meaning the potential exists for the contamination of eye exam equipment designed for repeat use. Further, cadaveric corneal transplants from undiagnosed CJD patients have led to two probable and three possible cases of disease transmission, the researchers say. Previous studies have shown that the eyes of CJD patients contain infectious prions, though the distribution of prions among the various components of the eye was not known. To address this question, the scientists recruited 11 CJD patients who agreed to donate their eyes upon death. The researchers found evidence of prion infection throughout the eyes of all 11 deceased patients using real time quaking-induced conversion (RT-QuIC), a highly sensitive test NIAID scientists developed that detects prion seeding activity in a sample as evidence of infection.

Keyword: Prions; Vision
Link ID: 25706 - Posted: 11.21.2018

By Kelly Servick SAN DIEGO, CALIFORNIA—If a diseased or injured brain has lost neurons, why not ask other cells to change jobs and pick up the slack? Several research teams have taken a first step by "reprogramming" abundant nonneuronal cells called astrocytes into neurons in the brains of living mice. "Everybody is astonished, at the moment, that it works," says Nicola Mattugini, a neurobiologist at Ludwig Maximilian University in Munich, Germany, who presented the results of one such experiment here at the annual meeting of the Society for Neuroscience last week. Now, labs are turning to the next questions: Do these neurons function like the lost ones, and does creating neurons at the expense of astrocytes do brain-damaged animals any good? Many researchers remain skeptical on both counts. But Mattugini's team, led by neuroscientist Magdalena Götz, and two other groups presented evidence at the meeting that reprogrammed astrocytes do, at least in some respects, impersonate the neurons they're meant to replace. The two other groups also shared evidence that reprogrammed astrocytes help mice recover movement lost after a stroke. Some see the approach as a potential alternative to transplanting stem cells (or stem cell–derived neurons) into the damaged brain or spinal cord. Clinical trials of that strategy are already underway for conditions including Parkinson's disease and spinal cord injury. But Gong Chen, a neuroscientist at Pennsylvania State University in State College, says he got disillusioned with the idea after finding in his rodent experiments that transplanted cells produced relatively few neurons, and those few weren't fully functional. The recent discovery that mature cells can be nudged toward new fates pointed to a better approach, he says. His group and others took aim at the brain's most abundant cell, the star-shaped astrocyte. © 2018 American Association for the Advancement of Science

Keyword: Stem Cells; Glia
Link ID: 25687 - Posted: 11.15.2018

Anna Azvolinsky In 1976, Huda Zoghbi (then Huda El-Hibri) was an eager first-year medical student at the American University of Beirut, Lebanon, her hometown. Halfway through that year, a civil war broke out. “Bombs were falling all around the medical campus,” the neuroscientist recalls. “I couldn’t commute 500 feet, let alone the two miles it took me to get home every day.” She and the other 62 students in her class decided that they, along with their professors, would live on campus—mostly underground, in double-walled rooms—to finish the school year. Although the medical school was considered a safe zone, as both warring factions would send their wounded there for care, an occasional bullet or piece of shrapnel still pierced the campus. One afternoon, Huda had ventured out for a walk on campus with her boyfriend, William Zoghbi, a fellow medical student. They were holding hands and for no particular reason let go. In those few seconds, a bullet flew between them. Neither was hurt, but the young couple realized in an instant how close and serious the war really was. Later, shrapnel wounded Huda’s younger brother while he was walking home from high school, so their parents decided to send them and another sibling to Texas, where their oldest sister was a professor of philosophy. The move was supposed to be temporary. But when the 1977 school year was to start in Lebanon, the civil war was still raging, and neither Huda nor her siblings could return home. © 1986 - 2018 The Scientist

Keyword: Movement Disorders; Genes & Behavior
Link ID: 25684 - Posted: 11.15.2018

David Cyranoski Japanese neurosurgeons have implanted ‘reprogrammed’ stem cells into the brain of a patient with Parkinson’s disease for the first time. The condition is only the second for which a therapy has been trialled using induced pluripotent stem (iPS) cells, which are developed by reprogramming the cells of body tissues such as skin so that they revert to an embryonic-like state, from which they can morph into other cell types. Scientists at Kyoto University use the technique to transform iPS cells into precursors to the neurons that produce the neurotransmitter dopamine. A shortage of neurons producing dopamine in people with Parkinson’s disease can lead to tremors and difficulty walking. In October, neurosurgeon Takayuki Kikuchi at Kyoto University Hospital implanted 2.4 million dopamine precursor cells into the brain of a patient in his 50s. In the three-hour procedure, Kikuchi’s team deposited the cells into 12 sites, known to be centres of dopamine activity. Dopamine precursor cells have been shown to improve symptoms of Parkinson’s disease in monkeys. Stem-cell scientist Jun Takahashi and colleagues at Kyoto University derived the dopamine precursor cells from a stock of IPS cells stored at the university. These were developed by reprogramming skin cells taken from an anonymous donor. “The patient is doing well and there have been no major adverse reactions so far,” says Takahashi. The team will observe him for six months and, if no complications arise, will implant another 2.4 million dopamine precursor cells into his brain. © 2018 Springer Nature Limited

Keyword: Parkinsons; Stem Cells
Link ID: 25682 - Posted: 11.14.2018

By Meredith Wadman A treatment for Niemann-Pick type C (NPC), an extremely rare and ultimately fatal neurodegenerative disease, performed no differently than placebo in a pivotal trial in 56 children and youths, its corporate sponsor announced on Tuesday. Perplexingly, though, the disease did not progress in either the treatment or placebo groups during the 1-year study, the company said. Normally, the condition, a result of impaired cholesterol metabolism, inexorably worsens, causing loss of balance, difficulty swallowing, seizures, and cognitive disabilities. The drug, VTS-270, a doughnut-shaped sugar molecule called a cyclodextrin, “did not show a statistically significant separation from placebo,” Steven Romano, Mallinckrodt Pharmaceuticals’s executive vice present and chief scientific officer told investors on a conference call on Tuesday. “But importantly, neither did [patients in the active or placebo arms of the trial] show disease progression as would have been anticipated in the neurodegenerative condition over 52 weeks of observation.” The drug was given by spinal injection into the cerebrospinal fluid, which circulates to the brain. The news—and the way Mallinckrodt, which has its U.S. headquarters in St. Louis, Missouri, delivered it—came as a shock to families in the NPC community, who learned of it when investors began to tweet about it. (The company did email a letter to NPC disease groups on Tuesday. Mallinckrodt, whose stock is publicly traded, added in a statement emailed to Science that securities laws prevented the company from notifying patients sooner.) © 2018 American Association for the Advancement of Science

Keyword: Movement Disorders; Development of the Brain
Link ID: 25661 - Posted: 11.10.2018

By Karin Brulliard Veterans Affairs Secretary Robert Wilkie defended the agency’s ongoing experiments on dogs Friday and said he would continue to “reauthorize” them, eight months after Congress passed legislation limiting tests that are opposed by a bipartisan cast of lawmakers and several veterans’ groups. Speaking at the National Press Club, Wilkie rejected calls to end research that he said led to the invention in the 1960s of the cardiac pacemaker and the discovery in the late 1990s of a treatment for deadly cardiac arrhythmias. These days, he said, some of the testing is focused on spinal cord injuries. “I love canines,” Wilkie said. “But we have an opportunity to change the lives of men and women who have been terribly hurt. And until somebody tells me that that research does not help in that outcome, then I’ll continue.” Wilkie’s comments drew swift backlash from lawmakers who have criticized the experiments, which occur at three VA locations and are invasive and sometimes fatal to the dogs, as cruel and unnecessary. President Trump in March signed a spending bill that included language restricting such tests, and legislation has been proposed that would end all canine research at VA. “Having sustained catastrophic injuries on the battlefield, which included the loss of both my legs, I am acutely aware of the vital role dogs play in helping troops recover from war’s physical and psychological tolls,” said Rep. Brian Mast (R-Fla.), an Army veteran and co-sponsor of the legislation. “The VA has not executed what we wanted as intent, which is to bring this to an end in its entirety, so we will keep up the pressure." © 1996-2018 The Washington Post

Keyword: Animal Rights; Regeneration
Link ID: 25660 - Posted: 11.10.2018

By James Gorman David Hu was changing his infant son’s diaper when he got the idea for a study that eventually won him the Ig Nobel prize. No, not the Nobel Prize — the Ig Nobel prize, which bills itself as a reward for “achievements that make people laugh, then think.” As male infants will do, his son urinated all over the front of Dr. Hu’s shirt, for a full 21 seconds. Yes, he counted off the time, because for him curiosity trumps irritation. That was a long time for a small baby, he thought. How long did it take an adult to empty his bladder? He timed himself. Twenty-three seconds. “Wow, I thought, my son urinates like a real man already.” He recounts all of this without a trace of embarrassment, in person and in “How to Walk on Water and Climb up Walls: Animal Movements and the Robotics of the Future,” just published, in which he describes both the silliness and profundity of his brand of research. No one who knows Dr. Hu, 39, would be surprised by this story. His family, friends, the animals around him — all inspire research questions. His wife, Jia Fan, is a marketing researcher and senior data scientist at U.P.S. When they met, she had a dog, and he became intrigued by how it shook itself dry. So he set out to understand that process. Now, he and his son and daughter sometimes bring home some sort of dead animal from a walk or a run. The roadkill goes into the freezer, where he used to keep frozen rats for his several snakes. (The legless lizard ate dog food). “My first reaction is not, oh, it’s gross. It’s ‘Do we have space in our freezer,’” Dr. Fan said. He also saves earwax and teeth from his children, and lice and lice eggs from the inevitable schoolchild hair infestations. “We have separate vials for lice and lice eggs,” he pointed out. © 2018 The New York Times Company

Keyword: Movement Disorders; Evolution
Link ID: 25650 - Posted: 11.06.2018

Ian Sample Science editor Two men who were paralysed in separate accidents more than six years ago can stand and walk short distances on crutches after their spinal cords were treated with electrical stimulation. David Mzee, 28, and Gert-Jan Oskam, 35, had electrical pulses beamed into their spines to stimulate their leg muscles as they practised walking in a supportive harness on a treadmill. Doctors believe the timing of the pulses – to coincide with natural movement signals that were still being sent from the patients’ brains – was crucial. It appeared to encourage nerves that bypassed the injuries to form new connections and improve the men’s muscle control. In many spinal cord injuries a small portion of nerves remain intact but the signals they carry are too feeble to move limbs or support a person’s body weight. “They have both recovered control of their paralysed muscles and I don’t think anyone with a chronic injury, one they’ve had for six or seven years, has been able to do that before,” said Grégoire Courtine, a neuroscientist at the Swiss Federal Institute of Technology in Lausanne. “When you stimulate the nerves like this it triggers plasticity in the cells. The brain is trying to stimulate, and we stimulate at same time, and we think that triggers the growth of new nerve connections.” Mzee was paralysed in a gymnastics accident in 2010. He recovered the use of his upper body and some control of his right leg after intensive rehabilitation at a paraplegic centre in Zurich. Doctors there told him further improvement was unlikely, but after five months of training with electrical stimulation, he regained control of the muscles in his right leg and can now take a few steps without assistance. © 2018 Guardian News and Media Limited

Keyword: Regeneration; Robotics
Link ID: 25633 - Posted: 11.01.2018