Chapter 11. Emotions, Aggression, and Stress
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THINK twice before you tell that fib. By watching courtroom videos, a computer has learned to predict if someone is telling the truth or a lie. A machine learning algorithm trained on the faces of defendants in recordings of real trials, including that of Andrea Sneiderman (above) who was convicted of lying, correctly identified truth-tellers about 75 per cent of the time. Humans managed just 59.5 per cent. The best interrogators can reach 65 per cent. “We’re actually pretty bad lie detectors,” says Rada Mihalcea at the University of Michigan in Ann Arbor. Mihalcea and her colleagues took 121 videos from sources such as the Innocence Project, a non-profit group in Texas dedicated to exonerating people with wrongful convictions. This is superior to simulated conversation because the speakers are more invested in what they are saying. Transcriptions of the videos that included the speaker’s gestures and expressions were fed into a machine learning algorithm, along with the trial’s outcome. To hone it further, the team plans to feed in even more data. Such a system could one day spot liars in real-time in court or at airport customs, says Mihalcea, who will present the work at the International Conference on Multimodal Interaction this month in Seattle, Washington. © Copyright Reed Business Information Ltd.
Link ID: 21610 - Posted: 11.06.2015
Nancy Shute In September, we reported on a charming little study that found people who feel blue after watching sad videos have a harder time perceiving colors on the blue-yellow axis. Now the researchers may be feeling blue themselves. On Thursday they retracted their study, saying that errors in how they structured the experiment skewed the results. Shortly after the study was published online, commenters started looking skeptically at the results. And because the researchers had posted their data online, those commenters were able to run the numbers themselves. They didn't like what they found. As one blogger wrote: "A major problem is that the authors are claiming that they've found an interaction between video condition and color axis, but they haven't actually tested this interaction, they've just done a pair of independent t-tests and found different results." As the indefatigable crew at the Retraction Watch blog points out, it's not the first time scientists have messed this up. "This exact experimental oversight occurs all too often, according to a 2011 paper in Nature Neuroscience, which found that the same number of papers performed the procedure incorrectly as did it correctly." And there were other problems, too, such as not testing participants' color perception before the study. © 2015 npr
By Nicholas Bakalar A person with depression is at higher risk for heart disease, and a person with heart disease is at higher risk for depression. The link between the two diseases is complex and not entirely understood. Many of the effects of depression — feeling unable to exercise or eat properly, for example — and the behaviors associated with depression, like smoking and abusing alcohol, are well established risk factors for heart disease. Some studies have suggested that insomnia, another symptom of depression, may also increase the risk for cardiovascular illness. Depression can also make heart disease worse. Heart patients with depression may find it more difficult to take medications and comply with the behavioral demands of living with heart disease. Depression may also have destructive physiological effects on heart rhythm, blood pressure, stress hormone levels and blood clotting, studies have shown. These may be among the reasons why depressed patients with stable cardiovascular disease, or those who have survived a heart attack or had coronary bypass surgery, are at two to three times higher risk of dying than similar patients without depression. Treating depressed heart patients with drugs like Prozac may help. These drugs, known as selective serotonin reuptake inhibitors, or S.S.R.I.’s, in addition to relieving depression, have blood-thinning effects that may be beneficial against heart disease. “It is clear that treatment with an S.S.R.I. reduces cardiac mortality in depressed patients post heart attack,” said Dr. Steven P. Roose, a professor of psychiatry at Columbia. “What is not clear is whether the reduction in mortality results from the antidepressant effect of the medication or the anti-platelet effect of the medication.” © 2015 The New York Times Company
Your sense of smell might be more important than you think. It could indicate how well your immune system is functioning, a study in mice suggests. Evidence of a connection between the immune system and the olfactory system – used for sense of smell – has been building for some time. For instance, women seem to prefer the scent of men with different immune system genes to their own. Meanwhile, other studies have hinted that the robustness of your immune system may influence how extraverted you are. To investigate further, Fulvio D’Acquisto at Queen Mary University of London and his colleagues studied mice missing a recombinant activating gene (RAG), which controls the development of immune cells. Without it, mice lack a working immune system and some genes are expressed differently, including those involved in the olfactory system. “That rang bells, because people with immune deficiencies often lose their sense of smell,” says D’Acquisto. Systemic lupus erythematosus, an autoimmune disease in which the immune system mistakenly attacks tissues in the skin, joints, kidneys, brain, and other organs, is one such example. His team measured how long it took mice to find chocolate chip cookies buried in their cages. Those missing RAG took five times as long as normal mice. They also failed to respond to the scent of almond or banana, which mice usually find very appealing – although they did still react to the scent of other mice. Further study uncovered abnormalities in the lining of their noses; physical evidence that their sense of smell might be disrupted. © Copyright Reed Business Information Ltd.
Adam Cole Watch a scary movie and your skin crawls. Goose bumps have become so associated with fear that the word is synonymous with thrills and chills. But what on earth does scary have do to with chicken-skin bumps? For a long time, it wasn't well understood. Physiologically, it's fairly simple. Adrenaline stimulates tiny muscles to pull on the roots of our hairs, making them stand out from our skin. That distorts the skin, causing bumps to form. Call it horripilation, and you'll be right — bristling from cold or fear. Charles Darwin once investigated goose bumps by scaring zoo animals with a stuffed snake. He argued for the now accepted theory that goose bumps are a vestige of humanity's ancient past. Our ancestors were hairy. Goose bumps would have fluffed up their hair. When they were scared, that would have made them look bigger — and more intimidating to attackers. When they were cold, that would have trapped an insulating layer of air to keep them warm. We modern humans still get goose bumps when we're scared or cold, even though we've lost the advantage of looking scarier or staying warmer ourselves. And researchers have found that listening to classical music (or Phil Collins), seeing pictures of children or drinking a sour drink can also inspire goose bumps. There's clearly a link with emotion and reward, too. © 2015 npr
By Christian Jarrett Neuroscientists, for obvious reasons, are really interested in finding out what’s different about the brains of people with unpleasant personalities, such as narcissists, or unsavory habits, like porn addiction. Their hope is that by studying these people’s brains we might learn more about the causes of bad character, and ways to helpfully intervene. Now to the list of character flaws that've received the brain-scanner treatment we can apparently add sexism — a new Japanese study published in Scientific Reports claims to have found its neurological imprint. The researchers wanted to know whether there is something different about certain individuals’ brains that potentially predisposes them to sexist beliefs and attitudes (of course, as with so much neuroscience research like this, it’s very hard to disentangle whether any observed brain differences are the cause or consequence of the trait or behavior that’s being studied, a point I’ll come back to). More specifically, they were looking to see if people who publicly endorse gender inequality have brains that are anatomically different from people who believe in gender equality. In short, it seems the answer is yes. Neuroscientist Hikaru Takeuchi at Tohoku University and his colleagues have identified two brain areas where people who hold sexist attitudes have different levels of gray-matter density (basically, a measure of how many brain cells are packed into a given area), as compared with people who profess a belief in gender equality (their study doesn’t speak to any subconsciously held sexist beliefs). What’s more, these neural differences were correlated with psychological characteristics that could help explain some people’s sexist beliefs. © 2015, New York Media LLC.
Bret Stetka Sometime around 1907, well before the modern randomized clinical trial was routine, American psychiatrist Henry Cotton began removing decaying teeth from his patients in hopes of curing their mental disorders. If that didn't work he moved on to more invasive excisions: tonsils, testicles, ovaries and, in some cases, colons. Cotton was the newly appointed director of the New Jersey State Hospital for the Insane and was acting on a theory proposed by influential Johns Hopkins psychiatrist Adolph Meyer, under whom Cotton had studied, that psychiatric illness is the result of chronic infection. Meyer's idea was based on observations that patients with high fevers sometimes experience delusions and hallucinations. In 1921 he published a well-received book on the theory called The Defective Delinquent and Insane: the Relation of Focal Infections to Their Causation, Treatment and Prevention. A few years later The New York Times wrote, "eminent physicians and surgeons testified that the New Jersey State Hospital for the Insane was the most progressive institution in the world for the care of the insane, and that the newer method of treating the insane by the removal of focal infection placed the institution in a unique position with respect to hospitals for the mentally ill." Eventually Cotton opened a hugely successful private practice, catering to the infected molars of Trenton, N.J., high society. © 2015 npr
By Diana Kwon Microglia, the immune cells of the brain, have long been the underdogs of the glia world, passed over for other, flashier cousins, such as astrocytes. Although microglia are best known for being the brain’s primary defenders, scientists now realize that they play a role in the developing brain and may also be implicated in developmental and neurodegenerative disorders. The change in attitude is clear, as evidenced by the buzz around this topic at this year’s Society for Neuroscience (SfN) conference, which took place from October 17 to 21 in Chicago, where scientists discussed their role in both health and disease. Activated in the diseased brain, microglia find injured neurons and strip away the synapses, the connections between them. These cells make up around 10 percent of all the cells in the brain and appear during early development. For decades scientists focused on them as immune cells and thought that they were quiet and passive in the absence of an outside invader. That all changed in 2005, when experimenters found that microglia were actually the fastest-moving structures in a healthy adult brain. Later discoveries revealed that their branches were reaching out to surrounding neurons and contacting synapses. These findings suggested that these cellular scavengers were involved in functions beyond disease. The discovery that microglia were active in the healthy brain jump-started the exploration into their underlying mechanisms: Why do these cells hang around synapses? And what are they doing? © 2015 Scientific American
The invaders put on a disguise and infiltrate the nest with dark plans: to kill the queen and enslave the kingdom. Usually when ants take pupae from other colonies as future slaves all hell breaks loose in ensuing battles. The enslaved individuals sometimes even strike back against their overlords. It’s a relatively dramatic affair, usually resulting in the aggressive slave-makers carrying the pupae back to their own colony, says Terrence McGlynn at California State University. But a species of ant found in the eastern US, Temnothorax pilagens, does things differently. It is the first ant species known to waltz into a colony and enslave others without killing, and one of a few that take not only pupae but adult workers, too. “This was extremely surprising as ants are usually able to detect foreign species or even individuals from a different colony through their chemical profile and react aggressively towards them,” says Isabelle Kleeberg at Johannes Gutenberg-Universität Mainz, Germany, whose team has found how they get away with it. Kleeberg tracked the behaviour of T. pilagens and their preferred slave species, Temnothorax ambiguus, in 43 raiding experiments using colour-marked individuals. In each experiment the colonies of these two ant species, each housed in a plastic box, were placed 12 centimetres apart from each other. © Copyright Reed Business Information Ltd.
What if belief in God and prejudice against immigrants could be altered by magnetic energy? That’s the question researchers sought to explore in a study published Wednesday in the journal Social Cognitive and Affective Neuroscience. The “magnetic energy” comes in the form of transcranial magnetic stimulation (TMS), a noninvasive procedure that uses a metal coil to send pulses to the brain. By activating certain regions of the brain, doctors have used it for things like measuring the damage of a stroke or—increasingly—treating depression. These researchers sought to do the opposite—to temporarily disable one part of the brain (the part that responds to threats) and measure its effect on beliefs and prejudices connected to them. To do this, researchers from Britain’s University of York teamed up with UCLA to find 39 politically moderate college undergraduates who were divided into two groups. The first was given a “love-level sham” dose of TMS that had no effect on their brains. The second got a hit of magnetic energy strong enough to temporarily shut down their posterior medial frontal cortex. The pMFC, as this area near the forehead is known, is the part of the brain that identifies problems and—after measuring the level of threat—generates a response to them. Testing the effect of shutting down the part of the brain that forms judgments based on threats required first presenting threats. After receiving their respective doses of TMS, participants were asked to respond to questions about their own death. Previous studies have shown the threat of death is capable of directly affecting a person’s belief in religion. Therefore, shutting down the part of the brain that registers this threat—they theorized—would reduce the need to believe in God.
Link ID: 21525 - Posted: 10.17.2015
Could brain inflammation be to blame for schizophrenia? People with the disorder seem to have more active immune cells inside their brains, and now this activity has been spotted even before the disorder develops. This link could be a breakthrough in developing new treatments that better target the causes of the disorder. The idea that the immune system might play a part in schizophrenia was first floated 10 years ago. Since then, a couple of studies have found that people with schizophrenia seem to have more active microglia – the immune cells of the brain. Peter Bloomfield at Imperial College London wondered if this increased immune system activity might be detectable before a person is diagnosed with schizophrenia. His team examined 14 people who had been identified as being at “ultra-high risk” of developing the disorder – they had already seen a doctor about symptoms like paranoia or hallucinations, but hadn’t yet had a psychotic episode. Typically, between 20 and 35 per cent of such individuals will go on to be diagnosed with schizophrenia. By injecting a dye that labels active cells and using a PET scanner, Bloomfield’s team compared the activity of these people’s microglial cells with those of people with schizophrenia, as well as healthy people. They found increased microglial activity in both those who had schizophrenia, and those who had been classified as ultra-high risk. “What’s interesting is that the level of activity correlated with the severity of symptoms,” says Bloomfield. During the study, two of the 14 at ultra-high risk went on to develop schizophrenia and schizotypal disorder – these people had the highest levels of microglial activity, says Bloomfield. © Copyright Reed Business Information Ltd.
By ANDREW SOLOMON INEXPLICABLE violence is the hardest kind to accept. The human wish to insert logic where there is none often drives bystanders to psychic violence of their own. This happened again last week, after it was reported that the shooter at Umpqua Community College in Oregon, Christopher Harper-Mercer, who killed nine people and injured several others, may have been autistic. Although there is no established connection between autism and murder, some eagerly leapt to causality and scapegoating. The killer’s “diagnosis” was based primarily on posts on Yahoo made over the last decade by his mother, Laurel Harper, in which she characterized both herself and her son as having Asperger’s syndrome — a category no longer in medical use that describes autistic people with advanced verbal skills. Mr. Harper-Mercer attended a school that caters to children with special needs, including autism. While Ms. Harper is not a doctor, her descriptions of her son across his childhood are consistent with the syndrome. A Facebook page called “Families Against Autistic Shooters” ranted about “the soulless, dead eyes of autistic children,” and characterized them as “cold, calculating killing machines with no regard for human life!” Its author announced: “What do all shooters over the last few years have in common? A lack of empathy and compassion due to Autism!” If Mr. Harper-Mercer were rumored to have been diabetic or afflicted with male-pattern baldness, no such “explanations” of his behavior would have surfaced. But despite a huge increase in awareness of autism among the public, those with the condition are often subject to this type of disparagement. This was evident in both the Facebook page and the response to it by Facebook’s management, who, despite the site’s anti-bullying policy, initially refused to remove it on grounds that it did not target named individuals. “Families Against Autistic Shooters” remained accessible until last Monday, by which time escalating media attention and a petition on Change.org with nearly 5,000 signatures embarrassed administrators into action. For the time it was viewable, the page stigmatized a population far more likely to be attacked than to attack, far less likely to receive justice when injured, and far more likely to be misunderstood. © 2015 The New York Times Company
A new drug for multiple sclerosis can cut relapses by almost 50% more than the current standard treatment, its manufacturer claims, raising the hopes of sufferers of the disease. The Swiss pharmaceutical giant Roche announced the headline results for its drug, ocrelizumab, but has not published the detailed outcome of its trials. The announcement was warmly welcomed by patients, not least because Roche claims the drug also has an impact on a form of the disease, called primary-progressive, which affects 10-15% of people with MS in the UK and for which there are no treatments. Roche claimed it cut disability in those patients by nearly a quarter. “These phase three trial results will provide a great deal of hope for people with primary-progressive MS, who currently don’t have any treatments available that can slow down the worsening of their condition,” said Nick Rijke, the MS Society’s executive director for policy and research. “Finding effective treatments for multiple sclerosis is our number one priority at the MS Society and this is a big moment. The drug was compared in the trials with Rebif, an established drug made by Merck that reduces relapses by about a third. Ocrelizumab – which does not yet have a brand name – was said to cut annual relapses by 46% and 47% compared with Rebif in the two trials. The biggest advantage, however, may be that it is claimed to cause fewer side effects than the established drug. © 2015 Guardian News and Media Limited
By Erika Hayasaki For 40 years, Joel Dreyer was a respected psychiatrist who oversaw a clinic for troubled children, belonged to an exclusive country club, and doted on his four daughters and nine grandchildren. Then, suddenly, he became a major drug dealer. Why? In the 1980s, psychiatrist Joel Dreyer was a fixture on Detroit’s WXYZ Channel 7. His commercials promoting his treatment center, InnerVisions, which he named after the Stevie Wonder album, sometimes ran up to five times a day. In one ad, Dreyer blocks a bartender from serving a mug of beer to a patron and says, “Don’t let your marriage or your job suffer from alcohol or drugs.” In another, Dreyer, in a navy pinstriped suit with a white pocket square, looks into the camera, his expression concerned and sympathetic. “Don’t you want to talk to someone who will listen?” he asks. “Someone who won’t pass judgment? Someone who cares? Come talk to me.” InnerVisions, which was based in Southfield, a suburb northwest of Detroit, had a staff of 80 physicians, psychologists, and therapists and took up two floors of a high-rise. It had made Dreyer not only a public figure but also wealthy. He maintained a side career as an expert witness. Attorneys called on him because he was smart, charming, and persuasive. Dreyer mostly testified for the defense, and with each high-profile case, his celebrity grew. Between the clinic, trial work, and his private practice, he was earning as much as $450,000 a year. Dreyer loved to be the center of attention. He would sometimes ride to work on a motorcycle in a bejeweled Elvis outfit to entertain his colleagues.
Allison Aubrey We might not be able to remember every stressful episode of our childhood. But the emotional upheaval we experience as kids — whether it's the loss of a loved one, the chronic stress of economic insecurity, or social interactions that leave us tearful or anxious — may have a lifelong impact on our health. In fact, a study published this week in the Journal of the American College of Cardiology indicates that emotional distress during childhood — even in the absence of high stress during adult years — can increase the risk of developing heart disease and metabolic disorders such as diabetes in adulthood. Robert Wood Johnson Foundation Shots - Health News Take The ACE Quiz — And Learn What It Does And Doesn't Mean "We know that the childhood period is really important for setting up trajectories of health and well-being," explains Ashley Winning, an author of the study and postdoctoral research fellow in social and behavioral sciences at the Harvard T.H. Chan School of Public Health. To assess the connection between childhood stress and the risk of disease, Winning and her colleagues analyzed data from the 1958 British Birth Cohort Study, a long-running study that documented the diets, habits and emotional health of thousands of British children born during the same week that year. As the children entered school, the classroom became the laboratory for observation. © 2015 NPR
By Nicholas Bakalar Agitation and aggression are common in Alzheimer’s patients, and there is no known safe and effective treatment. Now researchers report that a combination drug already in use for treating certain neurological problems may be a better remedy. Dextromethorphan is a cough suppressant commonly found in over-the-counter cough medicines, and quinidine is a drug used to control heart rhythm disorders. In combination, they are used to treat certain neurological disorders involving involuntary movement of the facial muscles. The scientists randomized 152 Alzheimer’s patients to a 10-week course of dextromethorphan-quinidine and 127 to placebo. Researchers then rated them using a well-validated scale that measures aggression and agitation. The study is in the Sept. 22 issue of JAMA. Aggression scores declined to 3.8 from 7.1 in the dextromethorphan-quinidine group and to 5.3 from 7.0 in those who took a placebo. Then the researchers re-randomized those who did not respond to placebo to receive either drugs or placebo, and found similar encouraging results for the drug combination. “Fifty-five percent of the people who were on drugs had a 50 percent reduction in their agitation,” said the lead author, Dr. Jeffrey L. Cummings, director of the Cleveland Clinic Lou Ruvo Center for Brain Health. “That’s a lot when a patient is striking and hitting and cussing. There are no currently approved treatments for agitation, and we’re very enthusiastic about this finding.” © 2015 The New York Times Company
By Sarah C. P. Williams Looking at photos of starving refugees or earthquake victims can trigger a visceral sense of empathy. But how, exactly, do we feel others’ agony as our own? A new study suggests that seeing others in pain engages some of the same neural pathways as when we ourselves are in pain. Moreover, both pain and empathy can be reduced by a placebo effect that acts on the same pathways as opioid painkillers, the researchers found. “This study provides one of the most direct demonstrations to date that first-hand pain and pain empathy are functionally related,” says neurobiologist Bernadette Fitzgibbon of Monash University in Melbourne, Australia, who was not involved in the new research. “It’s very exciting.” Previous studies have used functional magnetic resonance imaging (fMRI) scans to show that similar areas of the brain are activated when someone is in pain and when they see another person in pain. But overlaps on a brain scan don’t necessarily mean the two function through identical pathways—the shared brain areas could relate to attention or emotional arousal, among other things, rather than pain itself. Social neuroscientist Claus Lamm and colleagues at the University of Vienna took a different approach to test whether pain and empathy are driven by the same pathways. The researchers first divided about 100 people into control or placebo groups. They gave the placebo group a pill they claimed to be an expensive, over-the-counter painkiller, when in fact it was inactive. This well-established placebo protocol is known to function similarly to opioid painkillers, while avoiding the drugs’ side effects. © 2015 American Association for the Advancement of Science.
By Sarah C. P. Williams When the human body needs extra energy, the brain tells fat cells to release their stores. Now, for the first time, researchers have visualized the nerves that carry those messages from brain to fat tissue. The activation of these nerves in mice, they found, helps the rodents lose weight—an observation that could lead to new slimming treatments for obese people. “The methods used here are really novel and exciting,” says neuroendocrinologist Heike Muenzberg-Gruening of Louisiana State University’s Pennington Biomedical Research Center in Baton Rouge, who was not involved in the new study. “Their work has implications for obesity research and also for studying these nerves in other tissues.” Diagrams of the chatter between the brain and fat tissues have long included two-way arrows: Fat cells produce the hormone leptin, which travels to the brain to lower appetite and boost metabolism. In turn, the brain sends signals to the fat cells when it’s time to break down their deposits of fatty molecules, such as lipids, into energy. Researchers hypothesized that there must be a set of nerve cells that hook up to traditional fat tissue to carry these messages, but they’d never been able to indisputably see or characterize them. Now they have. Thanks to two forms of microscopy, neurobiologist Ana Domingos, of the Instituto Gulbenkian de Ciência in Oeiras, Portugal, produced images showing bundles of nerves clearly enveloping fat cells in mice. She and her colleagues went on to show, using various stains, that the nerves were a type belonging to the sympathetic nervous system that stretches outward from the spinal cord and keeps the body’s systems in balance. © 2015 American Association for the Advancement of Science
Link ID: 21448 - Posted: 09.26.2015
Dark puffy eyes, a feeling of deep exhaustion, and a foul mood to match – we’ve all experienced the side effects of a lack of sleep. It’s no wonder that sleep-deprivation has been used as a method of torture. Our brains seem to lose the ability to distinguish between the innocuous and emotional in such circumstances, turning us into overreacting, exhausted wrecks. We all know that a good night’s sleep is vital for a day of clear thinking, but exactly why sleep is so important remains a mystery. Talma Hendler of Tel Aviv University in Israel is particularly interested in how lack of sleep leaves us with a short emotional fuse. “We know that sleep affects our emotional behaviour, but we don’t know how,” she says. To investigate further, Hendler and her colleagues kept 18 adults awake all night. “It took a great effort,” she says. “During the night, we repeatedly measured their sleepiness, and unsurprisingly they got more and more tired.” The volunteers were put through two rounds of tests while their brains were scanned, both the day after a good night’s sleep and after being awake for 24 hours. In one test, volunteers were asked to give the direction in which yellow dots moved on a screen. In each case, the dots were laid over a potentially distracting picture that was either positively emotional (of a kitten or a couple in love, for example), negatively emotional (such as a mutilated body or a snake) or neutral (such as a cow or spoon). © Copyright Reed Business Information Ltd.
Ian Sample Science editor Government lawyers are seeking to block compensation payments to people who developed the devastating sleep disorder, narcolepsy, as a result of a faulty swine flu vaccine. The Pandemrix vaccine made by GlaxoSmithKline (GSK) was given to 6 million people in Britain and millions more across Europe during the 2009-10 swine flu pandemic, but was withdrawn when doctors noticed a rise in narcolepsy cases among those who received the jab. In June, a 12-year-old boy was awarded £120,000 by a court that ruled he had been left severely disabled by narcolepsy caused by Pandemrix. The win ended a three-year battle with the government that argued his illness was not serious enough to warrant compensation. Narcolepsy is a permanent condition that can cause people to fall asleep dozens of times a day, even when they are in mid-conversation. Some suffer from night terrors and a problem with muscular control called cataplexy that can lead them to collapse on the spot. The boy, who remains anonymous, has become disruptive at school because he is so tired and finds it almost impossible to socialise. He needs to take several naps in the school day and cannot shower unattended or take a bus alone. He may never be able to drive as an adult. © 2015 Guardian News and Media Limited