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News Article | April 12, 2016
Site: http://www.biosciencetechnology.com/rss-feeds/all/rss.xml/all

Results of a small study of people with tingling pain in their hands and feet have added to evidence that so-called prediabetes is more damaging to motor nerves than once believed, in a report on the study published online in JAMA Neurology on April 11. Johns Hopkins neurologists say the study of patients with small fiber neuropathy showed unexpected deterioration over the entire length of sensory nerve fibers, rather than just at the longest ends first, which the investigators say defies the conventional wisdom of how nerves were thought to deteriorate. Over the three-year course of the study of the 62 participants, 13 of them with prediabetes, the investigators found that generalized damage occurs in those with prediabetes, and that the precursor condition may be less benign than most clinicians appreciate. “I liken small fiber neuropathy to the canary in the coal mine,” said senior author Michael Polydefkis, M.D., professor of neurology at the Johns Hopkins University School of Medicine and director of the Cutaneous Nerve Lab. “It signals the beginning of nerve deterioration that with time involves other types of nerve fibers and becomes more apparent and dramatically affects people’s quality of life. The results of this new study add urgency to the need for more screening of those with the condition and faster intervention.” Small diameter nerve fibers reach out to the surface of the skin, and their damage is often marked by development of burning pain in the feet. But routine nerve tests, like nerve conduction, and routine examinations often fail to identify nerve damage because those measurements mostly assess injury to large diameter nerve fibers. The most common cause of small fiber neuropathy is diabetes, Polydefkis notes, but it can also be caused by lupus, HIV, Lyme disease, celiac disease or alcoholism. In an effort to measure damage more accurately in small nerve fibers in people with small fiber neuropathy symptoms, Polydefkis and his team took small samples of skin — the size of a large freckle — from 52 patients diagnosed with small fiber neuropathy and from 10 healthy controls. Of the 52 patients enrolled in the study with small fiber neuropathy, 13 were considered to have prediabetes, 14 had type 2 diabetes, and 25 had normal blood sugar and an unknown cause of neuropathy. The participants ranged in age from their mid-40s to late 60s, and just less than half were female. Skin samples were taken from the ankle, the lower thigh near the knee and the upper thigh. Three years later, samples from the same area in the same group were taken for comparison. Microscopic analysis of the skin samples was done to determine the density of small nerve fibers over time. According to the lead author of the study, Mohammad Khoshnoodi, M.D., assistant professor of neurology at Johns Hopkins, a lower density of fibers indicates more nerve damage. Initially, he said, all patients with small fiber neuropathy had fewer nerve fibers at the test site on the ankle compared to the upper thigh, demonstrating more nerve damage the further down the leg measured. After three years, all three groups of those with small fiber neuropathy lost nerve fibers at the site tested in the ankle. But what surprised the researchers was that nerve fibers were lost at similar rates from the lower and upper thigh sites as well, a phenomenon that would not have been expected if the longest nerve fibers were the most vulnerable. “We are all taught in medical school that the longest nerves degrade first, and we show that this isn’t always the case,” said Khoshnoodi. Patients with prediabetes or diabetes had at least 50 percent fewer small nerve fibers in their ankles initially than those participants with an unknown cause for their small fiber neuropathy, indicating these patients started the study with more damage to their small nerve fibers. The patients with prediabetes continued to have worsening damage to their small nerve fibers over the course of the study; they lost about 10 percent of their nerve fiber density each year at all sites tested along the leg. Patients with diabetes also lost similar rates of nerve fibers along the three sites of the leg. “I expected that people with diabetes would do worse, but I didn’t really expect people with prediabetes to experience a similar rate of degradation of their small nerve fibers,” said Polydefkis. Khoshnoodi cautions that the study was small, and that other factors in addition to high blood sugar, such as smoking, high blood pressure and high cholesterol, may also have contributed to the decline. Future studies that address these risk factors will need to be performed to determine if prediabetes is as debilitating to nerves as full-blown diabetes. According to the National Institute of Neurological Disorders and Stroke, an estimated 20 million people in the U.S. have some form of peripheral neuropathy. About 50 percent of people with diabetes have neuropathy.


News Article
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Using mice whose front paws were still partly disabled after an initial induced stroke, Johns Hopkins researchers report that inducing a second stroke nearby in their brains let them “rehab” the animals to successfully grab food pellets with those paws at pre-stroke efficiency. The findings, described online Dec. 31, 2015, in Neurorehabilitation and Neural Repair, show that the “window of opportunity” for recovering motor function after a stroke isn’t permanently closed after brain damage from an earlier stroke and can reopen under certain conditions, in conjunction with rapid rehabilitation efforts. The investigators strongly emphasize that their experiments do not and will never make a case for inducing strokes as a therapy in people with stroke disability. But they do suggest the mammalian brain may be far more “plastic” in such patients, and that safe and ethical ways might be found to better exploit that plasticity and reopen the recovery window for people who have never fully regained control of their motor movements. “If we can better understand how to reopen or extend the optimal recovery period after a stroke, then we might indeed change how we treat patients for the better,” said Steven Zeiler, M.D., Ph.D., assistant professor of neurology at the Johns Hopkins University School of Medicine. “Our study adds new strong and convincing evidence that there is a sensitive period following stroke where it’s easiest to relearn motor movements — a topic that is still debated among stroke researchers.” The new mouse experiments build on a previous study at Johns Hopkins, which found that the window of optimal recovery following a stroke in mice was within the first seven days, but this time period could be extended by giving mice the common antidepressant fluoxetine immediately after the stroke. The investigators suspected that the antidepressant increased the brain’s response to learning. Until now, however, the researchers say, there was no evidence that once the optimal period was over — with or without fluoxetine — the potential for recovery could be reopened. For the new research, which did not involve the use of the antidepressant, the researchers — as in their first experiments — taught mice to reach through a slit in their cage with their front paw to grasp food pellets affixed to a bar, a task that four-legged animals don’t naturally perform. Once the mice became efficient at the task — it took about 10 days of training — the researchers measured their individual success rates. On average, they found the mice successfully grabbed pellets just over 50 percent of the time. The researchers then induced a stroke in the motor cortex of the mice’s brains, making them unable to perform the task. After waiting a week — well beyond the known “optimal” window during which rehab training will work — they put the mice through almost three weeks of task training, during which the mice successfully grabbed the pellets again, but only about 30 percent of the time. For the next phase of the experiment, the scientists built on previous research and observations in mice that brain ischemia — the cutoff or reduction of oxygen to the brain during a stroke or other insult to the cortex — under certain conditions increased brain plasticity, the ability of the brain to compensate for injury and form new connections. To that end, the scientists induced a second stroke in the lab mice either in the secondary motor cortex near the first stroke site or, for purposes of a control group, in the visual cortex, located far from the original site. Instead of waiting days, the investigators began retraining these mice the next day and found that mice with the follow-up stroke in the motor cortex relearned to grasp the food pellets just as well as they did before the first stroke, with success more than 50 percent of the time. Mice in the control group never did any better, even with extended training, suggesting that the motor cortex may be the only part of the brain with this type of “reopening” capability for motor movements, the investigators say. Zeiler plans to investigate other ways to reopen the window of recovery and make use of the optimal recovery window. The lead investigator of the study, John Krakauer, M.D., M.A., professor of neurology, directs the Brain, Learning, Animation and Movement Lab, which uses basic science data, like that in this study, to develop new patient therapies. Currently, the lab is investigating the importance of early and intense rehabilitation in patients to enhance brain plasticity after stroke. According to the Centers for Disease Control and Prevention, in the U.S., stroke is the No. 1 cause of disability and costs $34 billion each year in in health care, medications and missed days of work. Funding for the study was provided by grants from the National Institute of Neurological Disorders and Stroke , the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the James S. McDonnell Foundation.


News Article
Site: http://news.yahoo.com/science/

Shoe inserts, back-support belts and other gadgets aimed at preventing low back pain may be a waste of money. Instead, exercise is the best way to ward off this common problem, a new review of studies suggests. The researchers found evidence that an exercise program alone, or exercise along with education about how to prevent back pain, was effective in averting an episode of low back pain and reducing people's use of sick time at work. Education may include receiving training in proper lifting techniques, learning about correct posture or attending back school, which is a comprehensive program on back health. About 80 percent of U.S. adults will experience an episode of low back pain at some point in their lives, according to the National Institute of Neurological Disorders and Stroke. [Lower Back Pain: Causes, Relief and Treatment] To evaluate which preventive methods for low back pain are effective in easing its discomfort, the researchers analyzed data from 23 studies with a total of nearly 31,000 participants. The analysis found that exercise alone could reduce a person's risk of low- back pain by 35 percent, and it could also cut the use of sick time by 78 percent over the course of a year. People who participated in an exercise program and also received additional educational instruction were 45 percent less likely to have low back pain over the course of one year, compared with people who were not involved in both programs, according to the research, published online today (Jan. 11) in the journal JAMA Internal Medicine. This means that the effect of exercise alone or in combination with education is quite large: It cuts a person's risk of getting low back pain in half, said study author Daniel Steffens, a chronic back pain researcher at the University of Sydney in Australia. But not all of the approaches for thwarting an aching back were deemed worthwhile. The study found that education alone, back belts (worn to protect the back from injury when lifting), shoe insoles and ergonomic adjustments (programs that modify a work station or redesign the steps involved in completing a task) were not effective in preventing back pain or reducing time off from work because of it. In other words, several strategies that have been believed to prevent low back pain seem not to provide a protective effect, Steffens told Live Science. The trials that the researchers evaluated in their review tested a variety of exercise programs that were designed to improve people's flexibility, posture, aerobic fitness and the strength of their back and core muscles, Steffens said. The programs did not just focus on the back, but included the upper and lower limbs as well, he said. The length of the exercise sessions varied, but participants typically did two to three group sessions per week with supervised instruction, and they also agreed to practice the techniques at home, Steffens said. The exercise programs lasted anywhere from eight weeks to 18 months. Although the reduced risk of back pain lasted for up to a year, beyond this time period, the preventative effect of exercise in combination with education was reduced, and the effect of exercise alone disappeared altogether, the analysis found. To have a lasting impact on preventing back pain, an ongoing exercise program is required, the researchers suggest. This review provides concrete evidence on the value of exercise for preventing back pain, wrote back-pain researchers Dr. Timothy Carey and Janet Freburger, of the University of North Carolina at Chapel Hill, in an editorial accompanying the study in the same issue of JAMA Internal Medicine. If a medication or injection were available that reduced the recurrence of low back pain to the extent seen in this review from exercise, we would be reading the marketing materials in medical journals and viewing them on television, said Carey and Freburger, who were not involved in the review. "However, formal exercise instruction after an episode of lowback pain is uncommonly prescribed by physicians," according to the editorial. Copyright 2016 LiveScience, a Purch company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.


News Article
Site: http://news.yahoo.com/science/

A woman's sudden delusions — including becoming wrongly convinced that her husband of 20 years was being unfaithful — turned out to have a surprising cause: a large cyst in her brain, according to a recent report of her case. The 43-year-old woman in Turkey had become suddenly suspicious of her husband's infidelity, and had started looking through his phone and personal belongings, the doctors who treated her wrote in their report of her case, published in March in the journal BMJ Case Reports. The woman came to see doctors in January 2015, seeking medical help for her paranoia about her husband's behavior, said Dr. C. Onur Noyan, a psychiatrist at NPIstanbul Neuropsychiatry Hospital in Istanbul who treated the woman and was the lead author of the case report. [16 Oddest Medical Cases] The woman reported having trouble sleeping and had become anxious and irritable, the authors wrote in the report. She had also recently experienced a stressful event: Her daughter had switched schools because she had been struggling academically, the authors noted. However, the woman had never experienced any psychiatric or neurological problems in the past, nor had anyone in her family, according to the report. The doctors conducted a detailed psychiatric evaluation and concluded that the woman had experienced a brief psychotic attack, Noyan said. In medicine, "psychotic" refers to a loss of contact with reality, such as delusions or hallucinations. Because she had never experienced such an attack before, the doctors ran additional tests, including brain scans, to see if they could find the biological cause of her symptoms, he said. A magnetic resonance imaging (MRI) scan revealed a large cyst, known as a porencephalic cyst, in the right frontal lobe of her brain. Such cysts form in the structural tissue of the brain, and are filled with cerebrospinal fluid, according to the report. "Porencephalic cysts are very rare" and are typically diagnosed in infants, Noyan said. Indeed, babies with porencephalic cysts are usually diagnosed by their first birthday, according to the National Institute of Neurological Disorders and Stroke; some do not live past age 20. The cysts are typically caused by a stroke or brain damage before or after birth, and can lead to symptoms such as seizures, muscle weakness and learning disabilities, according to the report. The cysts can occur anywhere in the brain, Noyan told Live Science. People's symptoms may differ depending on the location of the cyst, he added. In this woman, the cyst's location in her frontal lobe, which is involved in thinking and decision making, may have contributed to her psychosis, according to the report. [10 Things You Didn't Know About the Brain] While Noyan has seen porencephalic cysts in his practice before, he'd never seen one as large as this woman's, he said. In addition, the age at which the woman's first symptoms arose made the case unique, according to the report. There was no safe way to surgically remove the woman's cyst. To treat her, the doctors prescribed an anti-psychotic drug, which the woman will likely have to take for the rest of her life. Noyan last saw the patient about a month ago, and said that she is doing very well. She currently has no symptoms of psychosis and probably will not experience any psychotic attacks in the future, he said. Copyright 2016 LiveScience, a Purch company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.


News Article | October 5, 2015
Site: www.financialexpress.com

There is a telling vignette in Arun Maira’s interesting new book, An Upstart in Government. Maira was a member of the Planning Commission in the rank of minister of state between 2009 and 2014. A consultancy group made a presentation to then Prime Minister Atal Bihari Vajpayee on the nine steps that his government should take to ratchet up growth to 9% per annum. Vajpayee heard them out and then observed: “We know all this. The question is how will it be done.” Vajpayee put his finger on our leadership’s deepest dilemma. They know what is wrong. They know what must be done. But they do not know quite how to do it. The problem is that they are running out of time. People are losing patience with the explanation that it is the vagaries of democracy and the labyrinthine procedures of bureaucracy that stall the needle of change. Worldwide, public support is drifting towards the left and right extremes of the political spectrum. This is because of a growing sense that the mainstream centrist politicians are doing nothing to correct the tilt towards the “one percenters”—those with incumbent resources, skills and power and against the interests of the rest—and to bridge the deepening income divide. This drift is leading to the emergence of a new breed of politicians who are contemptuous of political convention and who are championing social and economic nationalism. This breed is receiving unexpected public acclaim. Donald Trump is a standout example. Last year, when he announced his candidacy for US president, he was the jokey butt of almost every talk show. His anti-immigration, protectionist, racist and sexist pronouncements were not expected to strike a chord. Today, he is leading the pack of hopefuls for the Republican Party presidential nomination. Jeremy Corbyn is another case. A few months back, he was an irrelevant, aged Labour Party backbencher. There were few who thought he could muster the support of 35 MPs—a requirement for contesting the Labour Party leadership. His extreme leftwing, eurosceptic, anti-Nato and anti-nuclear positions were deemed extreme and a recipe for unelectability. As it happened, he not only secured the 35 signatures (just) but also won the election. Greek Prime Minister Alexis Tsipras offers another example. He, too, is anti-establishment and leftwing. His re-election cocks a snook at the advocates of “responsible economics”. All of these examples are reflective of a subterranean current of fear at the tension between the opportunities offered by an open internet shared economy and the uncertainties of an international order riven by civil war, terrorist threat, refugee influx and cyber espionage. It reflects doubt at the ability of the conventional mainstream political leadership to manage this tension. There is a message in these trends for our leadership. Last week, our TV and print media carried commentaries of global CEOs, economists, Silicon Valley entrepreneurs, think-tankers and others on what should be done to restore India’s standing as a favoured haven for private investment. This was in the run up to and during the visit of Prime Minister Narendra Modi to the US. They said nothing that had not been heard before. Or that was not known to him and his able advisors. Or, indeed, that is not already on the agenda of the government. Infrastructure must be improved, bureaucracy must back off, procedures should be simplified, factor markets (labour, capital and land) should be structured to operate more efficiently, the fiscal regime must be transparent, predictable and stable, contract terms must be respected. So on and so forth. Still, it was important that they said what they did. For it contained a subtle message. The needle of change must be shifted more sharply, democracy is not an acceptable cover for non-performance, and if worldwide trends are anything to go by, there will be social and political consequences if the current gap between promise and delivery is not bridged quickly. So the perennial question. What is to be done? Clearly, we must not dispense with democracy. That is our bulwark and it needs to be nurtured. We should, of course, debate whether the Westminster first-past-the-post system needs to be reviewed. But this debate, if ever triggered, would be contentious and long. And in the meantime, frustrations will mount. The government cannot afford an idle parlour game. So the focus should be on our other systemic blocker: the bureaucracy. Maira offers another telling vignette. He wanted to hire two people from outside the Planning Commission to infuse new ideas. There was no budgetary allocation and the inter-ministerial approval process was too time-consuming. So he persuaded the Tata Group and Mahindra to “second” two of their executives at no cost to the commission. He then discovered that there was no mechanism for hiring individuals to do specific jobs. Only consultant organisations could be hired and that too following a competitive bid. So the two secondees were asked to form a consultancy organisation. This organisation submitted a “no cost” bid. They were told this would attract undue attention and that they should put in a number. They eventually won the contract with a R1 lakh charge. Maira commented: “Things are never simple in a procedure-bound bureaucracy.” Maira got what he wanted because of persistence and jugaad. But, as I am sure he will admit, this allows for only a temporary fix. It cannot compel a systemic change. For that to happen, the bureaucracy has to undergo a root and branch overhaul of its procedures and conduct rules. The Administrative Reforms Commission reports offers a blueprint. Maira himself has left behind an implementation model for the Niti Aayog. There are other experts who have written on the subject. The point is that this must now be the focus of the prime minister. He does not need legislative support. He has the administrative background. He is technologically savvy. The simplification of the nature and system of bureaucratic governance should be his new mantra. The author is chairman, Brookings India and senior fellow, Brookings Institution First Published on October 05, 2015 12:21 am

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