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Sara Reardon Like ivy plants that send runners out searching for something to cling to, the brain’s neurons send out shoots that connect with other neurons throughout the organ. A new digital reconstruction method shows three neurons that branch extensively throughout the brain, including one that wraps around its entire outer layer. The finding may help to explain how the brain creates consciousness. Christof Koch, president of the Allen Institute for Brain Science in Seattle, Washington, explained his group’s new technique at a 15 February meeting of the Brain Research through Advancing Innovative Neurotechnologies initiative in Bethesda, Maryland. He showed how the team traced three neurons from a small, thin sheet of cells called the claustrum — an area that Koch believes acts as the seat of consciousness in mice and humans1. Tracing all the branches of a neuron using conventional methods is a massive task. Researchers inject individual cells with a dye, slice the brain into thin sections and then trace the dyed neuron’s path by hand. Very few have been able to trace a neuron through the entire organ. This new method is less invasive and scalable, saving time and effort. Koch and his colleagues engineered a line of mice so that a certain drug activated specific genes in claustrum neurons. When the researchers fed the mice a small amount of the drug, only a handful of neurons received enough of it to switch on these genes. That resulted in production of a green fluorescent protein that spread throughout the entire neuron. The team then took 10,000 cross-sectional images of the mouse brain and used a computer program to create a 3D reconstruction of just three glowing cells. © 2017 Macmillan Publishers Limited
Geoff Brumfiel When the half-brother of North Korean leader Kim Jong Un collapsed at a Malaysian airport last week, poisoning was instantly suspected. But on Friday, Malaysian authorities revealed that an autopsy had turned up not just any poison, but a rare nerve agent known as VX. VX is among the deadliest chemical weapons ever devised. A colorless, odorless liquid, similar in consistency to motor oil, it kills in tiny quantities that can be absorbed through the skin. A relative of the nerve agent Sarin, VX disrupts communications between nerves and muscles. Victims of VX initially experience nausea and dizziness. Without an antidote, the chemical eventually paralyzes the diaphragm, causing suffocation. That may have been the fate of Kim Jong Nam, the estranged half-brother of North Korea's leader. Security footage showed that Kim was approached by two women who appeared to cover his face with a cloth. Moments later, he fell ill and sought help. He died before reaching a hospital. If the Malaysian analysis is correct and VX was the culprit, that would seem to suggest that the North Korean state itself is behind the killing. "Hardly anybody has it," says Dan Kaszeta, a chemical weapons expert and consultant based in London. The U.S. has destroyed nearly all of its stocks of VX in recent years. North Korea is among the few states in the world that have an active chemical weapons program. It is not a signatory to the Chemical Weapons Convention, which bans the use of such weapons. © 2017 npr
Link ID: 23282 - Posted: 02.25.2017
By James Gallagher Health and science reporter, Maps have revealed "hotspots" of schizophrenia and other psychotic illnesses in England, based on the amount of medication prescribed by GPs. The analysis by the University of East London showed North Kesteven, in Lincolnshire, had the highest rates. The lowest rate of schizophrenia prescriptions was in East Dorset. However, explaining the pattern across England is complicated and the research team says the maps pose a lot of questions. They were developed using anonymous prescription records that are collected from doctors' surgeries in England. They record only prescriptions given out by GPs - not the number of patients treated - so hospital treatment is missed in the analysis. Data between October 2015 and September 2016 showed the average number of schizophrenia prescriptions across England was 19 for every 1,000 people. Prof Allan Brimicombe, one of the researchers from UEL, said: "The pattern is not uniformly spread across the country." He suggests this could be due to "environmental effects" such as different rates of drink or drug abuse. Prof Brimicombe told the BBC: "The top one is in the Lincolnshire countryside and there are others in the countryside." © 2017 BBC
Link ID: 23281 - Posted: 02.25.2017
By Joshua A. Krisch When Kathleen Gardiner first encountered female mice with Down syndrome, she was surprised to find that the rodents’ brains showed unexpected abnormalities. Gardiner, a neuroscientist at the University of Colorado School of Medicine in Aurora, knew that trisomic male mice typically had perturbed protein levels in their hippocampuses. But these trisomic female mice showed the most serious changes in their cerebellums. “Right away, there’s a brain region sex difference,” Gardiner said. “It’s very interesting to ponder the fact that this could lead to sex differences in the learning, memory, or behavioral abnormalities associated with [Down syndrome].” Although Gardiner recognized that differences between mouse sexes would not necessarily translate into sex differences in humans, she considered the potential implications for clinical studies on Down syndrome therapies. “If we find that males or females are differing not only in their baseline impairment, but in their response to drugs, we need to know that,” she said. “We could be missing a big piece of information that could lead to better or different clinical trials.” Indeed, sex differences in model organisms are becoming increasingly apparent. Studies have shown sex differences in mice can affect cardiovascular health, liver disease, and cancer risk. Many of these studies are now published in Biology of Sex Differences, where Gardiner’s own work on the trisomic female mice appeared. © 1986-2017 The Scientist
By Carolyn Gramling Trilobites—three-sectioned, crablike critters that dominated the early Paleozoic—are so abundant that they have become the gateway fossil for most collectors. But paleontologists have found little evidence of how the extinct arthropods reproduced—until now. Researchers studying a fossil specimen of the trilobite Triarthrus eatoni spotted something odd just next to the animal’s head: a collection of small (about 200 micrometers across), round objects (in light blue, above). Those, they determined, are actually eggs—the first time anyone had observed fossil trilobite eggs right next to the critters themselves. The structures were exceptionally well preserved, the eggs and exoskeletons of the trilobites replaced with an iron sulfide ore called pyrite. They came from the Lorraine Group, a rock formation that spans much of the northeastern United States and dates to the Ordovician period (about 485 million to 444 million years ago); it has long been a mecca for trilobite hunters because of the pyritization. The placement of the eggs is suggestive, the researchers report in the March issue of Geology: They hypothesize that trilobites released their eggs and sperm through a genital pore somewhere in the head—much like modern horseshoe crabs do today. One possible reason for the rarity of the find may be that the brooding behavior of T. eatoni was relatively unusual in the trilobite world: The species tended to prefer a harsh, low-oxygen environment, and may have kept a closer eye on their eggs than other trilobite species. But, the authors note, one idea this finding does lay to rest is that trilobites might reproduce via copulation—a titillating but little-regarded hypothesis based on the fact that trilobites are sometimes found clustered on top of one another. Instead, trilobites were most likely spawners—and, in fact, that clustering behavior may be another parallel to horseshoe crabs, which can climb on top of one another in competition to fertilize released eggs. © 2017 American Association for the Advancement of Science
Rae Ellen Bichell Initially, Clint Perry wanted to make a vending machine for bumblebees. He wanted to understand how they solve problems. Perry, a cognitive biologist at Queen Mary University of London, is interested in testing the limits of animal intelligence. "I want to know: How does the brain do stuff? How does it make decisions? How does it keep memory?" says Perry. And how big does a brain need to be in order to do all of those things? He decided to test this on bumblebees by presenting the insects with a puzzle that they'd likely never encounter in the wild. He didn't end up building that vending machine, but he did put bees through a similar scenario. Perry and his colleagues wrote Thursday in the journal Science that, despite bees' miniature brains, they can solve new problems quickly just by observing a demonstration. This suggests that bees, which are important crop pollinators, could in time adapt to new food sources if their environment changed. As we have reported on The Salt before, bee populations around the world have declined in recent years. Scientists think a changing environment is at least partly responsible. Perry and colleagues built a platform with a porous ball sitting at the center of it. If a bee went up to the ball, it would find that it could access a reward, sugar water. One by one, bumblebees walked onto the platform, explored a bit, and then slurped up the sugar water in the middle. "Essentially, the first experiment was: Can bees learn to roll a ball?" says Perry. © 2017 npr
By Claudia Wallis Dinosaurs, Star Wars, train schedules, Disney princesses, maps, LEGO—subjects such as these can become all-consuming passions for children on the autism spectrum. What therapists and educators often call “circumscribed” or “restricted” interests (or, more generously, “special” interests) make up a characteristic symptom of autism spectrum disorder (ASD). The current edition of psychiatry’s Diagnostic and Statistical Manual of Mental Disorders describes them as “highly restricted, fixated interests that are abnormal in intensity or focus.” Roughly 90 percent of high-functioning kids with ASD display at least one such interest during their elementary school years, according to a 2007 survey conducted at the Yale University Child Study Center, one of the few studies to have examined the topic. For a family with an affected child, this kind of narrow preoccupation can be tedious and exhausting. Imagine a kid who will talk about nothing but the exits on the New Jersey Turnpike or the Captain Underpants book series. (Both actual examples.) Therapists and educators have traditionally tried to suppress or modulate a child’s special interest, or use it as a tool for behavior modification: Keep your hands still and stop flapping, and you will get to watch a Star Wars clip; complete your homework or no Harry Potter. But what if these obsessions themselves can be turned into pathways to growth? What if these intellectual cul-de-sacs can open up worlds? That is the idea explored in the film Life, Animated, a contender for the Academy Award for Best Documentary this Sunday night. © 2017 Scientific American
Link ID: 23277 - Posted: 02.24.2017
Jon Brock What if I told you that we can now identify babies who are going to develop autism based on a simple brain scan? This, in essence, is the seductive pitch for a study published last week in the journal Nature, and making headlines around the world. Early identification and diagnosis is one of the major goals of autism research. By definition, people with autism have difficulties with social interaction and communication. But these skills take many years to develop, even in typically developing (i.e., non-autistic) children. Potential early signs of autism are extremely difficult to pick out amidst the natural variation in behaviour and temperament that exists between all babies. A brain scan for autism would be a major step forward. But is the hype justified? Are we really on the brink of a new era in autism diagnostics? Without wishing to detract from the efforts of everyone involved in the study, it’s important to look at the results critically, both in terms of the scientific findings and their potential implications for clinical practice. The study, led by Heather Cody Hazlett at the University of North Carolina, was part of a larger research program investigating the development of babies who have an older sibling with autism. Because autism runs in families, these babies are much more likely to develop autism than babies from the general population.
By KATHRYN SHATTUCK After his short film screened at the Sundance Film Festival in 2008, a euphoric Simon Fitzmaurice was walking the snowy streets of Park City, Utah, when his foot began to hurt. Back home in Ireland that summer, by then dealing with a pronounced limp, he received a shattering diagnosis: motor neuron disease, or M.N.D. (more commonly known in the United States as A.L.S., or Lou Gehrig’s Disease), a neurological disorder that causes increasing muscle weakness and eventual paralysis and is, in most cases, fatal. The doctor gave Mr. Fitzmaurice, then 33, three or four years to live. That might have been the end of any normal existence. But Mr. Fitzmaurice, by his own measure a “bit of a stubborn bastard,” was determined to leave his wife, Ruth, and their two young sons — with a third on the way — a legacy other than self-pity. The result is Mr. Fitzmaurice’s first feature film, and perhaps his salvation — “My Name Is Emily.” The movie, which opened in limited release in the United States on Feb. 17, stars Evanna Lynch, the airy Luna Lovegood of “Harry Potter” fame, as a teenage outlier in both her Dublin foster home and high school who goes on the lam with her only friend (George Webster) to free her father (Michael Smiley) from a mental hospital. The film — with gorgeous scenes of Ms. Lynch plunged, nymphlike, into a cerulean sea or riding shotgun through the emerald countryside in a canary-yellow vintage Renault — won for best cinematography when it debuted at the Galway Film Fleadh in 2015. “I am not trying to prove anything,” Mr. Fitzmaurice wrote in an email, before quickly reconsidering. “Actually, I am trying to prove something. I remember thinking, ‘I must do this to show my children to never give up.’” Mr. Fitzmaurice was writing with his hands when he began the script for “My Name Is Emily.” By the time he was finished, he was writing with his eyes. © 2017 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 23275 - Posted: 02.24.2017
Laurel Hamers Clusters of a toxic bacterial protein have a surprising structure, differing from similar clumps associated with Alzheimer’s and Parkinson’s in humans, scientists report in the Feb. 24 Science. These clusters, called amyloids, are defined in part by their structure: straight regions of protein chains called beta strands, folded accordion-style into flat beta sheets, which then stack up to form a fiber. That definition might now need to be broadened. “All the amyloids that have been structurally looked at so far have certain characteristics,” says Matthew Chapman, a biologist at the University of Michigan in Ann Arbor who wasn’t part of the work. “This is the odd amyloid out right now.” In the human brain, misfolded proteins can form amyloids that trigger neurodegenerative diseases. But amyloids aren’t always a sign of something gone wrong — some bacteria make amyloids to help defend their turf. In Staphylococcus aureus, for example, the PSMα3 protein assembles into amyloids that help the bacteria kill other cells. Previous research suggested that PSMα3 clusters were like any other amyloid. But researchers using X-ray crystallography found that instead of straight beta strands, the PSMα3 fiber was made up of curly structures called alpha helices that resemble an old-fashioned phone cord. The helices still formed a familiar fiber shape just like the beta strands did, but the sheets making up that fiber were rippled instead of flat. |© Society for Science & the Public 2000 - 2017.
Link ID: 23274 - Posted: 02.24.2017
By Diana Kwon Neuroscientists have long debated how itch and pain overlap in the nervous system. Although itch was once thought to arise from the same neurons that generate pain, later observations disputing this theory led many to believe these sensations had distinct neural circuits. In a study published today (February 22) in Neuron, researchers report that a subset of “itch-specific” nerve cells in the murine spinal cord are also involved in sensing pain, bringing the specificity theory into question. “We were surprised that contrary to what the field believes, neurons [in the spinal cord] coded for both pain and itch sensations,” coauthor Shuhao Sun, a neuroscience graduate student at Johns Hopkins University, told The Scientist. “[This] means there can be some crosstalk between these two sensations in the central nervous system.” Historically, the observation that pain could quell itch led many neuroscientists to subscribe to the intensity theory, which suggested that, in the same neurons, weak stimulation generated itch, while strong activation led to pain. However, this theory was largely abandoned around the 1980s when several groups discovered that weak painful stimuli did not lead to itch and that strong itch stimuli did not lead to pain. Instead, many researchers adopted the labeled-line theory, which proposed that there were separate neurons dedicated to each sensation. © 1986-2017 The Scientist
Keyword: Pain & Touch
Link ID: 23273 - Posted: 02.24.2017
Tina Hesman Saey Humans and Neandertals are still in an evolutionary contest, a new study suggests. Geneticist Joshua Akey of the University of Washington in Seattle and colleagues examined gene activity of more than 700 genes in which at least one person carried a human and a Neandertal version of the gene. Human versions of some genes are more active than Neandertal versions, especially in the brain and testes, the researchers report February 23 in Cell. In other tissues, some Neandertal versions of genes were more active than their human counterparts. In the brain, human versions were favored over Neandertal variants in the cerebellum and basal ganglia. That finding may help explain why Neandertals had proportionally smaller cerebellums than humans do. Neandertal versions of genes in the testes, including some needed for sperm function, were also less active than human varieties. That finding is consistent with earlier studies that suggested male human-Neandertal hybrids may have been infertile, Akey says. But Neandertal genes don’t always lose. In particular, the Neandertal version of an immunity gene called TLR1 is more active than the human version, the researchers discovered. Lopsided gene activity may help explain why carrying Neandertal versions of some genes has been linked to human diseases, such as lupus and depression (SN: 3/5/16, p. 18). Usually, both copies contribute equally to a gene’s total activity. Less robust activity of a version inherited from Neandertals might cause total activity to dip to unhealthy levels, for instance. |© Society for Science & the Public 2000 - 2017
By Alice Klein The proof is in the packaging. Making all cigarette packets look the same reduces the positive feelings smokers associate with specific brands and encourages quitting, Australian research shows. The findings come ahead of the UK and Ireland introducing plain tobacco packaging in May. Australia was the first nation to introduce such legislation in December 2012. Since then, all cigarettes have been sold in plain olive packets with standard fonts and graphic health warnings. The primary goal was to make cigarettes less appealing so that people would not take up smoking in the first place. But an added bonus has been the number of existing smokers who have ditched the habit. Between 2010 and 2013, the proportion of daily smokers in Australia dropped from 15.1 to 12.8 per cent – a record decline. The number of calls to quit helplines also increased by 78 per cent after the policy change. Brand betrayal This drop in smoking popularity can be partly explained by a loss of brand affinity, says Hugh Webb at the Australian National University in Canberra. People derive a sense of belonging and identity from brands, he says. For example, you may see yourself as a “Mac person” or a “PC person” and feel connected to other people who choose that brand. “Marketers are extremely savvy about cultivating these brand identities.” © Copyright Reed Business Information Ltd
By RONI CARYN RABIN Older adults who started sleeping more than nine hours a night — but had not previously slept so much — were at more than double the risk of developing dementia a decade later than those who slept nine hours or less, researchers report. The increased risk was not seen in people who had always slept more than nine hours. “We’re not suggesting you go wake up Grandpa. We think this might be a marker for the risk of dementia, not a cause” of the illness, said Dr. Sudha Seshadri, a professor of neurology at Boston University School of Medicine and the senior author of the study, in Neurology. Using data from 2,457 people, average age 72, who were part of a study in Framingham, Mass., the researchers found that those with a new habit of excessive slumber were at a greater risk of all forms of dementia, including Alzheimer’s, which is characterized by a buildup of beta amyloid, a toxic protein fragment that forms plaques in the brain. “My suspicion is that this is a compensatory mechanism: that at a time when amyloid is building up in the brain, people may be sleeping longer as the body is reacting and trying to remove it from the brain,” Dr. Seshadri added. © 2017 The New York Times Company
Link ID: 23270 - Posted: 02.24.2017
Bruce Bower Chimps with little social status influence their comrades’ behavior to a surprising extent, a new study suggests. In groups of captive chimps, a method for snagging food from a box spread among many individuals who saw a low-ranking female peer demonstrate the technique, say primatologist Stuart Watson of the University of St. Andrews in Fife, Scotland, and colleagues. But in other groups where an alpha male introduced the same box-opening technique, relatively few chimps copied the behavior, the researchers report online February 7 in the American Journal of Primatology. “I suspect that even wild chimpanzees are motivated to copy obviously rewarding behaviors of low-ranking individuals, but the limited spread of rewarding behaviors demonstrated by alpha males was quite surprising,” Watson says. Previous research has found that chimps in captivity more often copy rewarding behaviors of dominant versus lower-ranking group mates. The researchers don’t understand why in this case the high-ranking individuals weren’t copied as much. The spread of new behaviors in groups of monkeys and apes depends on a variety of factors — including an innovator’s social status, age and sex — that can interact in unpredictable ways. “That’s why social learning in groups is so interesting to study,” says Elizabeth Lonsdorf, a primatologist at Franklin & Marshall College in Lancaster, Pa., who did not participate in the research. |© Society for Science & the Public 2000 - 2017.
By Kerry Grens Brain scans of 3,242 volunteers aged four to 63 years old revealed that those diagnosed with attention deficit hyperactivity disorder (ADHD)—roughly half of the group—had smaller tissue volumes in five brain regions. Because the differences were largest between children, the researchers concluded that ADHD likely involves a delay in brain maturation. The study, published in The Lancet Psychiatry on February 15, is the largest of its kind to date, and the authors hope it will change public perception of the disorder. “I think most scientists in the field already know that the brains of people with ADHD show differences, but I now hope to have shown convincing evidence … that will reach the general public and show that it has [a basis in the brain] just like other psychiatric disorders,” geneticist and coauthor Martine Hoogman of Radboud University in the Netherlands told The Washington Post. “We know that ADHD deals with stigma, but we also know that increasing knowledge will reduce stigma.” Most pronounced among the brain differences between those with and without ADHD was the amygdala, important for emotional processing. “The amygdala is heavily connected to other brain regions. It is a kind of hub for numerous kinds of signaling around salience and significance of events,” Joel Nigg, a psychiatry professor at Oregon Health & Science University School of Medicine who was not part of the study, told CNN. “The bigger story here is that alterations in amygdala have not been widely accepted as part of ADHD, so seeing that effect emerge here is quite interesting.” © 1986-2017 The Scientist
Patricia Neighmond Many men over 65 with low testosterone levels say their sense of well-being, not to mention sexual function, isn't what it used to be. That's why some doctors prescribe testosterone replacement. But the effectiveness of testosterone has been controversial. Studies of the risks and benefits have been mixed, and the Food and Drug Administration beefed up its warnings about cardiac side effects of testosterone supplementation in 2015. And the findings of five studies released Tuesday aren't likely to clear up the confusion. They appear in JAMA, the journal of the American Medical Association and JAMA Internal Medicine. The studies are collectively called the Testosterone Trials (TTrials) and they compared a testosterone gel, AndroGel, against a placebo. The results are based on 788 men with below normal levels of testosterone studied at 12 sites across the country over a year. Overall, researchers saw improvements in bone density and bone strength in men who used a testosterone gel, which raised their testosterone to levels seen in younger men. In men with unexplained anemia, testosterone also improved iron levels in the blood. (A reviewer of the study raised questions about whether it was done ethically.) But in men using testosterone who had been reporting memory problems at the start of the study, there were no improvements in memory or cognition. And there were worrisome signs of an increase in the risk of cardiovascular problems. © 2017 npr
Daqing Li and Ying Li In 1969 Geoffrey Raisman, who has died aged 77, introduced the term “plasticity” to describe the ability of damaged nerve tissue to form new synaptic connections. He discovered that damaged nerves in the central nervous system (CNS) could be repaired and developed the theory that white matter (nerve fibres and supporting cells) is like a pathway – when it is disrupted by injury, such as spinal cord injury, growth of the regenerating fibres is blocked. In 1985 he described how olfactory ensheathing cells (OECs) “open doors” for newly formed nerve fibres in the nose to enter the CNS. Believing that reconstruction of the damaged pathway is essential to repair of the injured CNS and using the unique door-opening capability of OECs, in 1997, together with colleagues, Geoffrey showed that transplantation of OECs into the damaged spinal cord in experimental models repairs the damaged pathway and results in the regeneration of severed nerve fibres and the restoration of lost functions. The study led to a joint clinical trial with Pawel Tabakow and his team at Wroclaw Medical University, Poland. In 2014 the first patient with a complete severance of the thoracic spinal cord received transplantation of his own OECs. The operation enabled the patient, Darek Fidyka, to gain significant neurological recovery of sensation and voluntary movement. He can now get out of his wheelchair and ride a tricycle. The wider application of OECs has also been investigated. In 2012, with his team at University College London, collaborating with the UCL Institute of Ophthalmology and Southwest hospital, at the Third Military Medical University in Chongqing, China, Geoffrey described the protective effect of OECs in an experimental glaucoma model. The discovery has led to a plan to translate this research to clinical application which, it is hoped, will help many sufferers regain sight.
By Jennifer Couzin-Frankel At least two dozen junior and senior researchers are stuck in scientific limbo after being barred from publishing data collected over a 25-year period at a National Institutes of Health (NIH) lab. The unusual ban follows the firing last summer of veteran neurologist Allen Braun by the National Institute on Deafness and Other Communication Disorders (NIDCD) for what many scientists have told Science are relatively minor, if widespread, violations of his lab’s experimental protocol. Most of the violations, which were unearthed after Braun himself reported a problem, involve the prescreening or vetting of volunteers for brain imaging scans and other experiments on language processing. The fallout from the case was recently chronicled on a blog by one of Braun’s former postdocs, and it highlights a not-uncommon problem across science: the career harm to innocent junior investigators following lab misconduct or accidental violations on the part of senior scientists. But this case, say those familiar with it, is extreme. “We’re truly collateral damage,” says Nan Bernstein Ratner of the University of Maryland in College Park, who researches stuttering. She spent 5 years collaborating with Braun. Now, two of her graduate students have had to shift their master’s theses topics, and an undergraduate she mentored cannot publish a planned paper. “The process has been—you can use this term—surreal.” © 2017 American Association for the Advancement of Science
By Jessica Hamzelou Three people with paralysis have learned to type by thought alone using a brain implant – at the fastest speeds recorded using such a system. Two have motor neurone disease, also known as ALS – a degenerative disorder that destroys neurons associated with movement – while the other has a spinal cord injury. All three have weakness or paralysis in all of their limbs. There is a chance that those with ALS will eventually lose the ability to speak, too, says Jaimie Henderson, a neurosurgeon at Stanford University Medical Center in California. People who have lost the ability to talk may be offered devices that allow them to select letters on a screen using head, cheek or eye movements. This is how Stephen Hawking communicates, for example. But brain-machine interfaces are also being developed in the hope that they may one day be a more intuitive way of communicating. These involve reading brain activity, either externally or via an implant embedded in the brain, and turning it into a signal that can be used to direct something in the environment. At the moment, these devices are a little slow. Henderson and his colleagues wanted to make a device that was quicker and easier to use than those currently in trials. © Copyright Reed Business Information Ltd.