Ray Maota Brand Soputh Africa CEO Miller Matola (top right) and other industry leaders took part in the Lead SA Bok Friday initiative. Matola in his Bok jersey “played his part” to support the Boks. (Images: Ray Maota) MEDIA CONTACTS • Shelley Viljoen Primedia Broadcasting PR manager +27 11 506 3000 • Brand South Africa +27 11 483 0122 RELATED ARTICLES • Playing a part to back the Boks • Growing support for Play Your Part • New campaign for a better South Africa • New campaign to power South Africa’s ProteasSouth Africans have been mobilised to stand behind their beloved Springboks, the national rugby team, as they prepare to do battle in the 2011 Rugby World Cup.The tournament kicks off on 9 September – 23 October 2011.Brand South Africa showed its support by endorsing the Lead SA Bok Friday initiative at Primedia’s offices in Sandton, Johannesburg, on 26 August 2011.“We are proud of this initiative by Lead SA to garner support for our beloved Bokke and we as the IMC are proud to ‘play our part’ in bringing national pride back into sport,” Brand South Africa CEO Miller Matola said at the event.Brand South Africa launched its Play Your Part campaign in June 2011 as a call to citizens to do whatever they can, big or small, to try and make the country a better place to live in.The organisation was in Port Elizabeth on 20 August to support the Boks as they faced New Zealand in a Tri-Nations clash.The Boks winning the game helped boost national pride – just as the Play Your Part campaign aims to do.Lead SA also encourages citizens to make a difference in the country whichever way they can.Drumming up Bok Friday fever at PrimediaMatola was joined at the event by Absa marketing and communications executive Happy Ntshingila, Deputy Minister of Sport and Recreation Gert Oosthuizen and Lead SA CEO Yusuf Abramjee, who is also head of news and current affairs at Primedia.Well-known South African personalities, including Zuraida Jardin, Tumisho Masha, John Robbie, Danny K, Alex Jay and Pabi Moloi, also attended the event and showed their support for the Boks.Abramjee said: “With the call to citizens to support the Springboks by wearing Bok jerseys on Fridays, we are also proud to introduce Claudia Nel who won the Pretoria News art competition for Lead SA.”Nel is a pupil at Hoërskool Menlo Park in Pretoria.The competition called on South Africans to submit artwork that can be used on Lead SA postcards.Nel’s contribution, featured on the front page of the Pretoria News, showed a face in colours of the South African flag and the city skyline in the background.Adding his voice at the Primedia gathering, Absa’s Ntshingila said: “We as Absa have always supported the Boks and there’s nothing bigger and better than getting behind our national teams, as we saw during the 2010 Fifa World Cup.”Absa was an associate sponsor of the Boks for nine years before being named the official sponsor in March 2011 in a deal worth more than R50-million (US$6.9-million).The Boks will have a send-off party organised by Lead SA on 1 September at the Nelson Mandela Square in Sandton, where Danny K and La Vuvuzela will perform, among other artists.DStv’s Supersport channel will show the Rugby World Cup matches live and supply footage to other stations to ensure all 50-million South Africans behind the Boks.Rugby in South AfricaRugby has played a major transformational role in South Africa after the Springboks won the 1995 Rugby World Cup on home soil.The impressive victory by the Boks came a year after the first democratic elections in the country, which resulted in Nelson Mandela becoming president.The shot of Mandela and then-Bok captain Francois Pienaar hoisting the Webb-Ellis trophy at Ellis Park in Johannesburg has become an iconic national image.
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Reviewed by Alina Shrourou, B.Sc. (Editor)Oct 23 2018Using a novel biomarker panel to track and measure kidney function, researchers at University of California San Diego School of Medicine and University of California San Francisco School of Medicine report that lowering systolic blood pressure to less than 120 mm Hg does not damage the kidney organ itself. Instead, any negative changes to clinical results are more likely due to decreased blood flow.Previously, physicians believed significantly lowering high blood pressure in hypertensive patients damaged the kidneys.The findings are published in the October 23 issue of Annals of Internal Medicine.”There has always been debate surrounding how aggressively blood pressure should be treated since more aggressive treatment would require more medications and strain on the kidneys,” said Joachim H. Ix, MD, chief of the Division of Nephrology-Hypertension at UC San Diego School of Medicine. “However, we now have evidence that apparent changes in kidney function are predominantly the result of less blood flood, not damage.””The available tests that clinicians typically use to monitor kidney health are both antiquated and inadequate. The creatinine test results are leading clinicians to make the wrong decisions around blood pressure treatment,” said Michael G. Shlipak, MD, MPH, scientific director of the Kidney Health Research Collaborative at UC San Francisco School of Medicine. “There is an urgent need to bring new kidney tests into clinical practice, so that we can monitor the health inside the kidney.”The Systolic Blood Pressure Innovation Trial (SPRINT) was a large clinical trial that randomized hypertensive individuals to receive intensive blood pressure lowering to less than 120 versus standard of care. Using a subset of data from SPRINT, researchers designed a nested case-control study with 162 participants who did not develop chronic kidney disease (CKD). These patients were matched to SPRINT participants who had been diagnosed with incident CKD based on changes in serum creatinine — the main clinical marker of kidney function — during the course of the trial. By comparing nine urinary biomarkers that are known to mark intrinsic kidney damage, researchers were able to compare measurements between these groups at baseline and one-year of follow-up.Related StoriesMathematical model helps quantify metastatic cell behaviorScientists turn type A blood into universal type O, potentially doubling blood transfusion stocksCarbohydrate plays important role in regulating blood pressure, research suggests”More intensive blood pressure lowering to a target of 120 saves lives and prevents cardiovascular events, but this was previously counter-balanced by perceived risks of kidney,” said Ix. “The mortality and cardiovascular disease benefits are major reasons to consider being more aggressive with your blood pressure management. The new data suggest that this can be accomplished without any real damage to the kidneys.”Hypertension affects more than 100 million American adults. Uncontrolled over time, high blood pressure can cause narrowing of the arteries and slow or block blood flow to the kidneys. This can cause CKD. If untreated, CKD can lead to kidney failure.Ix said his team would like to conduct studies with longer follow-up, and extend their investigation to other conditions where treatments may cause blood flow changes to the kidney, but may not necessarily cause kidney damage.”We are excited to use the new biomarker panel on future studies to further define the differences in intrinsic kidney damage verses changes from a reduction in blood flow,” said Ix. “With close to 10 percent of Americans suffering from kidney disease, these future research studies could have a large impact.” Source:https://health.ucsd.edu/news/releases/Pages/2018-10-22-Kidneys-Arent-Harmed-When-Significantly-Lowering-Blood-Pressure.aspx?_ga=2.127351117.1392075183.1540311903-2119186239.1515157559
Source:http://www.sfn.org/ Reviewed by Kate Anderton, B.Sc. (Editor)Dec 25 2018Research suggests interventions designed to mitigate influence of low SES on brain and mental health may be most beneficial for children younger than age fiveThe relationship between socioeconomic status (SES) and brain anatomy is mostly stable from childhood to early adulthood, according to a longitudinal neuroimaging study of more than 600 healthy young people published in JNeurosci. This finding draws attention to the importance of preschool life as a period when associations between SES and brain organization may first develop.Related StoriesNeural pathways explain the relationship between imagination and willingness to helpNew network for children and youth with special health care needs seeks to improve systems of careResearch sheds light on sun-induced DNA damage and repairCassidy McDermott, Armin Raznahan, and colleagues analyzed brain scans of the same individuals collected over time between five and 25 years of age. Comparing this data to parental education and occupation and each participants’ intelligence quotient (IQ) allowed the researchers to demonstrate positive associations between SES and the size and surface area of brain regions involved in cognitive functions such as learning, language, and emotions. In particular, this is the first study to associate greater childhood SES with larger volumes of two subcortical regions – the thalamus and striatum – thereby extending previous SES research that has focused on its relationship to the cortex. Finally, the researchers identify brain regions underlying the relationship between SES and IQ. A better understanding of these relationships could clarify the processes by which SES becomes associated with a range of life outcomes, and ultimately inform efforts to minimize SES-related variation in health and achievement.
Source:http://www.kobe-u.ac.jp/research_at_kobe_en/NEWS/news/2019_02_08_01.html Reviewed by James Ives, M.Psych. (Editor)Feb 11 2019The bone marrow disease myelofibrosis is stimulated by excessive signaling from vitamin D and immune cells known as macrophages, reveals a Japanese research team. These findings could help to develop alternative treatments that do not target problem genes. The team was led by Research Fellow Kanako Wakahashi and Junior Associate Professor Yoshio Katayama (Kobe University Graduate School of Medicine) and the findings were published on February 4 in the online edition of Blood.There are three types of blood cell: white blood cells, red blood cells, and platelets. All three types are created from hematopoietic stem cells located in the bone marrow. Myelofibrosis causes an abnormal increase in the cells that produce collagen fibers called fibroblasts. The bone marrow becomes filled with these fibers, preventing the body from producing blood cells as normal. This condition can make it hard to control other diseases, and bone hardening (osteosclerosis) also occurs. Myelofibrosis occurs in blood tumors called myeloproliferative neoplasms, which are caused by genetic mutations of hematopoietic stem cells.The research team focused on the relationship between blood and bone. Vitamin D is a hormone that regulates calcium, and the team had already shown that vitamin D receptors control the location of hematopoietic cells in the bone marrow. In this study, the team performed a bone marrow (with vitamin D receptors) transplant for a mouse model without vitamin D receptors (this means it has a high concentration of vitamin D in the body) to create a myelofibrosis model. By analyzing this model, they found that hematopoietic stem cells were strongly stimulated by vitamin D signaling and grew into immune system cells called macrophages. These pathological macrophages stimulated young osteoblasts (cells that create bone) to induce myelofibrosis and bone hardening (figure 1). The cells known as fibroblasts are thought to be these young osteoblasts. By giving these mice a low vitamin D diet and suppressing the macrophages, the team was able to largely prevent the onset of myelofibrosis.Related StoriesLong-term follow-up of childhood cancer survivors is essential to maintain bone healthCommon antibacterial agent may be bad news for bone healthNew study sheds light on the role of vitamin D in muscle cellsThe team also examined mouse models with the same genetic disorder as myelofibrosis patients (JAK2V61F transgenic mice). These mice presented similar symptoms to myelofibrosis patients, displaying both fibrosis and bone hardening. They treated the mice by rearing them on a low vitamin D diet, blocking vitamin D receptor signals (removing the vitamin D receptor gene in blood cells) and suppressing macrophages. This proved to be extremely effective in preventing bone marrow fibrosis (figure 2).The results show that pathological macrophages produced by vitamin D receptor signaling play an important role in the development of myelofibrosis (figure 3). Clinical treatment uses inhibitors to target the causative genes of myeloproliferative tumors, but this is not always effective in treating myelofibrosis. Professor Katayama comments: “The only permanent cure for this disease is hematopoietic stem cell transplant, but this method is unsuitable for many elderly patients. These new findings may help to develop a treatment method for the elderly targeting the vitamin D pathway and macrophages.”
It turned out that on the molecular level, the process of aging in nematodes always unfolds in the same way, and all the observed differences in lifespan appear to reflect changes in the rate of aging. The researchers proposed that similar effects should be achievable without genetic interventions. To test the hypothesis, the researchers employed the Connectivity Map (CMAP) created by scientists at the Broad Institute of MIT and Harvard. CMAP contains information about the effect of almost all available FDA-approved drugs on gene activity in human cells. The researchers looked for drugs that alter human gene expression in a way opposing the age-related changes observed for corresponding genes in nematodes.Related StoriesNew protein target for deadly ovarian cancerComputers, games, crafting keep the aging brain sharpA Portable Solution for the On-scene Identification of KratomFrom the 1309 drugs in the CMAP database, the researchers chose 10 candidates that appear to act on genes in the desired direction. Six of these drugs had been previously documented anti-aging potential, while 4 of the shortlisted drugs had never been studied before in that context. The experiment demonstrated that all these drugs slow down aging in nematodes, albeit to different degrees. The most efficient compound extended the nematode lifespan by 30%.”This study resulted in several practical implications for aging research and the growing longevity industry. Firstly, we demonstrated that aging in nematodes is partially programmed and can be modified therapeutically. This might well hold true for other multicellular organisms, humans included. Secondly, we proposed a new method of searching life-extending compounds. The usual procedure involves laborious screening of large libraries of potential drugs. Unfortunately, even successful hits sometimes get missed by chance or due to non-optimal dosage. Our method allows for a targeted search of the compounds with the required activity, including FDA-approved drugs. The latter compounds have the advantage that they have already passed all the necessary clinical trials and can be used off-label as anti-aging drugs,” commented Andrei Tarkhov, Gero research scientist and a PhD candidate at Skolkovo Institute of Science and Technology.Robert Shmookler Reis, leader of the UAMS team, emphasized how extraordinary these results were. “Previous studies of pharmacologically active compounds (3) had found less than 1 out of 20 that were able to extend C. elegans lifespan, in striking contrast to our observation of life extension by 4 out of 4 drugs for which there were no previous aging data, selected only for transcriptomic signatures opposing those observed for aging of nematodes. This is remarkably compelling evidence that the expression profile of aging must be conserved from nematodes to humans, and is likely to be fundamental to all animals.”Source:Skolkovo Institute of Science and TechnologyJournal reference:Tarkhov, A.E. et al. (2019) A universal transcriptomic signature of age reveals the temporal scaling of Caenorhabditis elegans aging trajectories. Scientific Reports. doi.org/10.1038/s41598-019-43075-z. Our main concern was that aging in an extremely long-living worm might be totally different from that of normal, wild-type nematodes. In that case, the radical extension of lifespan would require complex interventions, and studies of animals with drastically slowed aging would not help us in our search for a truly effective anti-aging therapy.”Peter Fedichev, Principal Investigator, Gero/Skoltech/MIPT Group Reviewed by James Ives, M.Psych. (Editor)May 23 2019Researchers from Gero, Skolkovo Institute of Science and Technology (Skoltech), Moscow Institute of Physics and Technology (MIPT), and University of Arkansas for Medical Sciences (UAMS) collaborated to derive a transcriptomic signature of aging, which they confirmed using large transcriptomic databases. They discovered that aging in nematodes is partially programmed and can be therapeutically reversed by a number of FDA-approved drugs. The study is published in Scientific Reports.C. elegans, a nonparasitic roundworm, is one of the most intensively studied animals on Earth. Its genome was the first to be sequenced among multicellular organisms; each and every one of its almost thousand cells has been characterized by biologists. These nematodes normally have a short lifespan of 15-25 days, which makes them a convenient model organism for aging studies. However, their lifespan can be extended almost ten-fold by introducing a mutation to a single gene. Details remained unanswered, as to how such a dramatic intervention affects gene expression and aging to achieve this extension, and whether it can be mimicked therapeutically, ideally with the drugs already approved for human use.To answer this question, an international team of researchers led by Peter Fedichev, a founder of the longevity biotech startup Gero, required gene-activity data from nematodes with a wide variety of lifespans, at many ages across their lifespans. The UAMS researchers created the necessary strains (mutant worms in a constant, normal background) as well as normal, wild-type worms after suppression of selected target genes, and assessed their expression profiles at a range of adult ages. The Gero/Skoltech/MIPT scientists then leveraged machine learning techniques to analyze these experimental results and to compare them with earlier data available from public resources. The cost of the resulting dataset, named “MetaWorm”, is approaching $10 million and is a perfect example of scientific “data recycling”. Through analysis of the unique “MetaWorm” dataset, they confirmed and extended the pattern of transcriptomic shifts that accompany nematode aging.
This article was reprinted from khn.org with permission from the Henry J. Kaiser Family Foundation. Kaiser Health News, an editorially independent news service, is a program of the Kaiser Family Foundation, a nonpartisan health care policy research organization unaffiliated with Kaiser Permanente. Reviewed by Alina Shrourou, B.Sc. (Editor)Jun 12 2019After nearly 40 years as an internist, Dr. Ron Naito knew what the sky-high results of his blood test meant. And it wasn’t good.But when he turned to his doctors last summer to confirm the dire diagnosis — stage 4 pancreatic cancer — he learned the news in a way no patient should.The first physician, a specialist Naito had known for 10 years, refused to acknowledge the results of the “off-the-scale” blood test that showed unmistakable signs of advanced cancer. “He simply didn’t want to tell me,” Naito said.A second specialist performed a tumor biopsy, and then discussed the results with a medical student outside the open door of the exam room where Naito waited.”They walk by one time and I can hear [the doctor] say ‘5 centimeters,'” said Naito. “Then they walk the other way and I can hear him say, ‘Very bad.'”Months later, the shock remained fresh.”I knew what it was,” Naito said last month, his voice thick with emotion. “Once [tumors grow] beyond 3 centimeters, they’re big. It’s a negative sign.”The botched delivery of his grim diagnosis left Naito determined to share one final lesson with future physicians: Be careful how you tell patients they’re dying.Since August, when he calculated he had six months to live, Naito has mentored medical students at Oregon Health & Science University and spoken publicly about the need for doctors to improve the way they break bad news.”Historically, it’s something we’ve never been taught,” said Naito, thin and bald from the effects of repeated rounds of chemotherapy. “Everyone feels uncomfortable doing it. It’s a very difficult thing.”Robust research shows that doctors are notoriously bad at delivering life-altering news, said Dr. Anthony Back, an oncologist and palliative care expert at the University of Washington in Seattle, who wasn’t surprised that Naito’s diagnosis was poorly handled.”Dr. Naito was given the news in the way that many people receive it,” said Back, who is a co-founder of VitalTalk, one of several organizations that teach doctors to improve their communication skills. “If the system doesn’t work for him, who’s it going to work for?”Up to three-quarters of all patients with serious illness receive news in what researchers call a “suboptimal way,” Back estimated.”‘Suboptimal’ is the term that is least offensive to practicing doctors,” he added.The poor delivery of Naito’s diagnosis reflects common practice in a country where Back estimates that more than 200,000 doctors and other providers could benefit from communication training.Too often, doctors avoid such conversations entirely, or they speak to patients using medical jargon. They frequently fail to notice that patients aren’t following the conversation or that they’re too overwhelmed with emotion to absorb the information, Back noted in a recent article.”[Doctors] come in and say, ‘It’s cancer,’ they don’t sit down, they tell you from the doorway, and then they turn around and leave,” he said.That’s because for many doctors, especially those who treat cancer and other challenging diseases, “death is viewed as a failure,” said Dr. Brad Stuart, a palliative care expert and chief medical officer for the Coalition to Transform Advanced Care, or C-TAC. They’ll often continue to prescribe treatment, even if it’s futile, Stuart said. It’s the difference between curing a disease and healing a person physically, emotionally and spiritually, he added.”Curing is what it’s all about and healing has been forgotten,” Stuart said.The result is that dying patients are often ill-informed. A 2016 study found that just 5% of cancer patients accurately understood their prognoses well enough to make informed decisions about their care. Another study found that 80% of patients with metastatic colon cancer thought they could be cured. In reality, chemotherapy can prolong life by weeks or months, and help ease symptoms, but it will not stop the disease.Related StoriesNew protein target for deadly ovarian cancerUsing machine learning algorithm to accurately diagnose breast cancerResearch sheds light on sun-induced DNA damage and repairWithout a clear understanding of the disease, a person can’t plan for death, Naito said.”You can’t go through your spiritual life, you can’t prepare to die,” Naito said. “Sure, you have your [legal] will, but there’s much more to it than that.”The doctors who treated him had the best intentions, said Naito, who declined to publicly identify them or the clinic where they worked. Reached for verification, clinic officials refused to comment, citing privacy rules.Indeed, most doctors consider open communication about death vital, research shows. A 2018 telephone survey of physicians found that nearly all thought end-of-life discussions were important — but fewer than a third said they had been trained to have them.Back, who has been urging better medical communication for two decades, said there’s evidence that skills can be taught — and that doctors can improve. Many doctors bridle at any criticism of their bedside manner, viewing it as something akin to “character assassination,” Back said.”But these are skills, doctors can acquire them, you can measure what they acquire,” he said.It’s a little like learning to play basketball, he added. You do layups, you go to practice, you play in games and get feedback — and you get better.For instance, doctors can learn — and practice — a simple communication model dubbed “Ask-Tell-Ask.” They ask the patient about their understanding of their disease or condition; tell him or her in straightforward, simple language about the bad news or treatment options; then ask if the patient understood what was just said.Naito shared his experience with medical students in an OHSU course called “Living With Life-Threatening Illness,” which pairs students with ill and dying patients.”He was able to talk very openly and quite calmly about his own experience,” said Amanda Ashley, associate director of OHSU’s Center for Ethics in Health Care. “He was able to do a lot of teaching about how it might have been different.”Alyssa Hjelvik, 28, a first-year medical student, wound up spending hours more than required with Naito, learning about what it means to be a doctor — and what it means to die. The experience, she said, was “quite profound.””He impressed upon me that it’s so critical to be fully present and genuine,” said Hjelvik, who is considering a career as a cancer specialist. “It’s something he cultivated over several years in practice.”Naito, who has endured 10 rounds of chemotherapy, recently granted the center $1 million from the foundation formed in his name. He said he hopes that future doctors like Hjelvik — and current colleagues — will use his experience to shape the way they deliver bad news.”The more people know this, it doesn’t have to be something you dread,” he said. “I think we should remove that from medicine. It can be a really heartfelt, deep experience to tell someone this, to tell another human being.”
“The cost of smoking to the economy is huge – around £13 billion to the UK economy, including over £3 billion for NHS and social care and £7.5 billion to lost productivity. So these types of schemes could help save money as well as lives.”The team investigated whether rewards such as cash payments, vouchers, or the return of money deposited by those taking part, worked. The review summarizes the results from 33 randomized controlled trials involving more than 21,600 people from eight countries. They included ten trials that focused on pregnant smokers who were rewarded with vouchers for quitting and staying smoke-free.All of the trials in the general population followed participants for at least six months and those who quit were checked by testing their breath or bodily fluids.Some of the studies did not provide enough data for the team to fully assess their quality. But taking out the lowest quality trials from the analysis did not change the results.Related StoriesStudy reveals how habitual smoking may contribute to development of hypertensionStudy: Less than 50% of U.S. adults exposed to court-ordered anti-smoking advertisementsSmoking cessation during pregnancy associated with reduced risk of preterm birthThe researchers say that the certainty of their findings in the general population is high. Their certainty about the findings in pregnant women is moderate, as there weren’t as many studies and some were lower quality.Dr Notley said: “We found that six months or more after the beginning of the trials, people receiving rewards were approximately 50 per cent more likely to have stopped smoking than those in the control groups.”In people not receiving incentives, approximately seven per cent had successfully quit for six months or longer, compared to approximately 10.5 per cent of those receiving incentives.”This is an important increase when we consider the enormous harms of smoking, and benefits of quitting, and suggests that incentives can be a useful part of a comprehensive approach to help people quit smoking. Another really important thing is that success rates continued beyond when the incentives had ended.”The total financial amount of incentives varied considerably between trials, from zero (self-deposits), to a range of between £35 ($45 USD) and £912 ($1185).Dr Notley added: “For pregnant women, we also found that women in the rewards groups were more likely to stop smoking than those in control groups – both at the end of the pregnancy and after the birth of the baby, suggesting incentives may be a useful part of a comprehensive approach to helping pregnant women quit smoking.”Stopping smoking during pregnancy is the best thing that women can do to improve their chances of having a healthy pregnancy. Staying stopped after the birth has great benefits for babies too, through avoiding exposure to second hand smoke.”The review was led by UEA, and involved researchers from the University of Oxford and the University of Stirling.’Incentives for smoking cessation’ is published by the Cochrane Library on July 17, 2019. Source:University of East Anglia Reviewed by James Ives, M.Psych. (Editor)Jul 17 2019Financial incentives work to help people stop smoking and remain smoke free – according to research led by the University of East Anglia (UEA).Evidence published today in the Cochrane Library provides strong evidence that financial incentives helped people to stop smoking, and stay stopped long term.The review also found that incentives helped pregnant women stop smoking.Lead author Dr Caitlin Notley, from UEA’s Norwich Medical School: “We wanted to know whether these schemes actually work long term, as previously it was thought that perhaps incentives only worked for the time that they were given. We found that they do help people stay smoke free, even after the incentive scheme ends. Smoking is the leading cause of disease and death worldwide. Most smokers want to quit, but stopping smoking can be really challenging.Quitting smoking can greatly improve peoples’ health. Rewards, such as money or vouchers, have been used to encourage smokers to quit, and to reward them if they stay stopped. Such schemes have been used in workplaces, in clinics and hospitals, and within community programs.”
Japan’s crypto exchange to refund to customers after theft Citation: Japan to sanction Coincheck after massive cryptocurrency heist (2018, January 29) retrieved 18 July 2019 from https://phys.org/news/2018-01-japan-sanction-coincheck-massive-cryptocurrency.html The massive heist caused a loss of $530 million worth of the cryptocurrency NEM—based on the exchange rate on Friday—exceeding even the $480 million in bitcoin stolen from the MtGox exchange in 2014.Coincheck suspended trading of all cryptocurrencies except bitcoin on Friday, and said it had lost 523 million units of NEM, the 10th biggest cryptocurrency in the world based on market capitalisation.”The Financial Services Agency (FSA) will issue an order to improve operations, including protection of clients,” top government spokesman Yoshihide Suga said.The agency will supervise the exchange to ensure the measures are being implemented and contracts are being honoured, Suga told a regular briefing.”While examining the cause of the incident and taking necessary measures, we want the ministries and agencies concerned to urgently study what further measures we’d need,” he added.Coincheck said it would use its own funds to reimburse about 46.3 billion yen (around $430 million)—at a rate of 88.549 yen per NEM—to all 260,000 customers who lost their holdings.One unit of NEM was trading at 98 cents at around 0430 GMT on Monday, according to coinmarketcap.com.Japan is a leading market for cryptocurrencies, with nearly one third of global bitcoin transactions in December denominated in yen, according to specialist website jpbitcoin.com.As many as 10,000 businesses in Japan are thought to accept bitcoin, and bitFlyer, the country’s main bitcoin exchange, saw its user base grow beyond one million in November.Many Japanese, especially younger investors, have been seduced by the idea of strong profits as the economy has seen years of ultra-low interest rates offering little in the way of traditional returns.In the wake of the MtGox scandal, Japan passed a law on cryptocurrencies that requires exchanges to be regulated by the FSA.The law went into effect in 2017.Local media reported that Coincheck had submitted an application to the FSA for a licence and was allowed to continue operating while it awaited a decision. Japan said Monday it would impose administrative measures on virtual currency exchange Coincheck after hackers stole hundreds of millions of dollars in digital assets from the Tokyo-based firm. © 2018 AFP This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only. The massive Coincheck heist caused a loss of $530 million in the cryptocurrency NEM Explore further
The police alleges that Kumar had incited the mob to shout anti-India slogans on the university campus on February 9, 2016 to commemorate the hanging of Parliament-attack mastermind Afzal Guru terrorism (crime) The Delhi Police filed a chargesheet on Monday against former Jawaharlal Nehru University Students’ Union (JNUSU) president Kanhaiya Kumar and others in a sedition case lodged in 2016.The police also charged former JNU students Umar Khalid and Anirban Bhattacharya for allegedly shouting anti-India slogans during an event on the university campus on February 9, 2016 to commemorate the hanging of Parliament-attack mastermind Afzal Guru.The others chargesheeted in the case are Kashmiri students Aquib Hussain, Mujeeb Hussain, Muneeb Hussain, Umar Gul, Rayeea Rassol, Bashir Bhat and Basharat.As many as 36 others, including Communist Party of India (CPI) leader D Raja’s daughter Aprajita, Shehla Rashid (then vice-president of the JNUSU), Rama Naga, Ashutosh Kumar and Banojyotsna Lahiri have been named in column 12 of the chargesheet due to insufficient evidence against them, police sources said.Metropolitan Magistrate Sumit Anand put up the chargesheet for consideration before a competent court on Tuesday.The accused have been charged with offences under sections 124A (sedition), 323 (punishment for voluntarily causing hurt), 465 (punishment for forgery), 471 (using as genuine a forged document or electronic record), 143 (punishment for being a member of an unlawful assembly), 149 (being a member of an unlawful assembly), 147 (punishment for rioting) and 120B (criminal conspiracy) of the Indian Penal Code (IPC).The chargesheet also contains CCTV footage, mobile footage and documentary evidence.The police has alleged that Kumar had incited the mob to shout anti-India slogans.A case was registered on February 11, 2016 under sections 124A and 120B of the IPC against unidentified persons at the Vasant Kunj (North) police station, following complaints from Bharatiya Janata Party (BJP) MP Maheish Girri and the Akhil Bharatiya Vidyarthi Parishad (ABVP).The said event had taken place despite the university administration cancelling the permission, following a complaint from the ABVP, which had termed it as “anti-national”. RELATED JNU rusticates Umar, 2 others; Kanhaiya fined Rs 10,000 SHARE SHARE EMAIL COMMENTS Kanhaiya Kumar Published on Kanhaiya thanks Rahul for support in JNU row COMMENT SHARE January 14, 2019