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  • richardmitnick 7:34 am on October 7, 2015 Permalink | Reply
    Tags: , , , Medicine   

    From AAAS: “Nobel Prize honors drugs that fight roundworms, malaria” 



    5 October 2015
    Gretchen Vogel
    With reporting by Dennis Normile, Kathleen McLaughlin, and Christina Larson.

    William Campbell, Satoshi Ōmura, and Youyou Tu

    Three scientists have been awarded the 2015 Nobel Prize in Physiology or Medicine for decades-old findings that led to “revolutionary treatments” for devastasting diseases in the developing world. William Campbell of Drew University in Madison, New Jersey, and Satoshi Ōmura of Kitasato University in Tokyo share half of the prize for discovering avermectin, a drug to kill roundworms that cause blindness and deformities. The other half of the prize goes to Youyou Tu of the China Academy of Chinese Medical Sciences in Beijing, who discovered and refined artemisinin, which has proved highly effective against severe cases of malaria.

    “The global impact of the discovery and the impact on mankind is immeasurable,” Hans Forssberg, a neuroscientist and member of the Nobel Assembly, which selects the winners, said today at a press conference announcing the award.

    “It is extremely rewarding to know that people from the development community have been recognized for work that really helps people,” says David Molyneux, who heads the neglected tropical diseases program at the School of Tropical Medicine in Liverpool, U.K. Molyneux estimates that ivermectin, a derivative of avermectin, has been given more than a billion times, preventing more than 500,000 cases of blindness.

    Ōmura, a microbiologist, was searching for useful compounds from soil bacteria in Japan, and he developed methods for large-scale culturing and studying of these microbes. From thousands of cultures of Streptomyces, he identified some 50 that appeared to be strong candidates for antimicrobial drugs. Studying these strains, Campbell found that one was particularly effective at killing roundworms in farm animals and pets. The active component was purified and named avermectin. Subsequent versions have been so effective at curing the parasitic diseases river blindness and lymphatic filariasis—which causes gross deformities—that the diseases have been nearly eradicated.

    The key findings were described in these two papers, both published in 1979 in Antimicrobial Agents and Chemotherapy.

    The prize came as a big surprise to Ōmura. ”I humbly accept it,” he told the media arm of the Nobel Foundation in a telephone interview today. “I’m still not sure it’s quite right for me to receive this award,” he said later in an interview with the Japanese broadcasting company NHK. “There are many talented researchers in Japan. What I do is just tedious labor. I never really expected myself to be a Nobel laureate. I’ve always been proud that my work helped people, I tried to help people. But that is different from being a Nobel laureate.”

    “I’m in shock,” Campbell told ScienceInsider. Unlike the Nobel Peace Prize, scientific Nobels cannot be awarded to more than three people, he notes, “so I assumed there was no way the prize could be given for this, because it was a group effort.” Although team efforts are standard in science, he says, “this was a team of teams.”

    The path from Ōmura’s soil sample to a drug used in African villages was long, Campbell says, and there were few “Eureka” moments along the way. “One develops a very subdued form of excitement,” he says. “You don’t assume this is going to make it all the way to the marketplace or the clinic.”

    Pharmacologist Youyou Tu also found an important drug from natural sources. Searching though historical records of traditional Chinese medicine, she noticed that sweet wormwood was in hundreds of recipes for treating malaria. When she tested extracts in mice, she saw hints of an effect, but the studies were inconclusive. A recipe in a 1700-year-old book led Tu to a new method to extract the active compound. This turning point led to the drug artemisinin, which acts effectively on the early stage of the parasite’s life cycle. The drug has “remarkably reduced the death toll during last decades” for hundreds of millions of people infected with severe malaria, Forssberg said.

    Tu won the Lasker Award in 2011 for her work on artemisinin—the first Chinese scientist to get that award. But many scientists in China were outraged that she was singled out; they argued that the discovery was a mass effort involving thousands of researchers and that credit should not be Tu’s alone. The drug was borne of Project 523 (named for the 23 May 1967 date of its founding), an ambitious research arm of the People’s Liberation Army working on orders from Chairman Mao Zedong to find a cure for malaria.

    Historians say that Tu entered the research project later than other researchers, when many of her colleagues were exhausted by both their work and the ongoing political struggles that had engulfed China. Others defended Tu during the Lasker controversy, however. She has maintained a low profile herself.

    See the full article here .

    The American Association for the Advancement of Science is an international non-profit organization dedicated to advancing science for the benefit of all people.

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  • richardmitnick 3:46 pm on October 6, 2015 Permalink | Reply
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    From Outsmart Ebola Together at WCG: “Finding new avenues to attack Ebola” 

    New WCG Logo

    6 Oct 2015
    Dr. Erica Ollmann Saphire, PhD, The Scripps Research Institute

    Efforts to simulate matches between candidate compounds and one key Ebola virus protein are largely complete. Simulations of matches against another, newly discovered target protein are beginning now. Even as simulation work continues, the team is beginning to analyze these results and home in on compounds that could form the basis for effective new drugs against Ebola and other related diseases. Thanks to your help, and a new grant, the work is proceeding well.

    Two Protein Data Bank structures for the ribonuclease H domain of HIV reverse transcriptase. We used structural and experimental data for this domain to optimize our analysis protocols for the Lassa NP exonuclease site.

    Thanks to the efforts of thousands of World Community Grid members, my team has continued to make progress on Outsmart Ebola Together, a project whose goal is to find new drugs for curing Ebola and related life-threatening viral hemorrhagic fevers.

    Outsmart Ebola Together began with a study of potential drug attacks against the receptor-binding site of the Ebola surface glycoprotein (GP). We then announced the start of work on a second drug target: the nucleoprotein (NP) of Lassa Fever virus. Specifically, we are looking for drugs that attack the newly discovered “exonuclease site” of Lassa NP. This exonuclease site helps conceal the virus’s presence from the infected human cell by destroying the virus’s own excess production of double-stranded RNA.

    We have since prepared research tasks for testing the Lassa NP exonuclease site against millions of potential drugs. These tasks are now ready for use, and will be sent out to World Community Grid volunteers over the coming months.

    Our lab has also been investigating the Ebola NP and VP35 proteins. NP and VP35 must engage in a series of specific interactions with each other as Ebola virus replicates. These newly discovered interactions could potentially be disrupted by new drugs, making NP and VP35 possible future targets for investigation by Outsmart Ebola Together.

    At this stage in the project, we’ve gathered enough data that we need to begin focusing on analysis procedures for the data already returned by World Community Grid volunteers. We must analyze the data for both the Ebola GP receptor-binding site and the Lassa NP exonuclease site; and our analysis procedures must be sufficient to filter out false positives from the large quantity of results returned.

    For each viral protein site that we test against potential drugs, we assure the validity of our analysis as follows: We select a substantially analogous site (generally from a different virus) for which there exists experimental data about potential drugs that bind or do not bind to the site. We then tune our analysis protocols so that, when applied to this site, our analysis results closely match the known experimental results. Only when this is done do we feel that we can confidently apply the same analysis protocols to the site of current interest.

    In particular, this summer we looked closely at analysis optimization for the Lassa NP exonuclease site. As the analogous well-studied site, we chose the “ribonuclease H domain” of HIV reverse transcriptase, which has strong similarities to the Lassa NP exonuclease site in its protein structure and use of catalytic metal ions. The optimization of our analysis protocols against experimental data for the HIV ribonuclease H domain is now complete, and we are looking forward to the arrival of the Lassa NP exonuclease data as it is processed by World Community Grid volunteers. Candidate drugs that pass the analysis stage will go on to a next round of experiments, conducted in the lab rather than by computer simulation.

    We are also happy to announce that a $50,000 grant to support this work has been provided by the Robert Wood Johnson Foundation President’s Grant Fund of the Princeton Area Community Foundation. With this grant and the vast computing resources of World Community Grid, our way to the successful completion of the project is clear.

    As always, we close with a thank-you to the volunteers who have run this work for us. As you can see, we’ve already made significant progress but there is much work still to do. Make sure you’re signed up to contribute to this project, and spread the word about our lifesaving work!

    See the full article here.

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    World Community Grid (WCG) brings people together from across the globe to create the largest non-profit computing grid benefiting humanity. It does this by pooling surplus computer processing power. We believe that innovation combined with visionary scientific research and large-scale volunteerism can help make the planet smarter. Our success depends on like-minded individuals – like you.”

    WCG projects run on BOINC software from UC Berkeley.

    BOINC is a leader in the field(s) of Distributed Computing, Grid Computing and Citizen Cyberscience.BOINC is more properly the Berkeley Open Infrastructure for Network Computing.

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    “Download and install secure, free software that captures your computer’s spare power when it is on, but idle. You will then be a World Community Grid volunteer. It’s that simple!” You can download the software at either WCG or BOINC.

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    The Clean Energy Project

    Discovering Dengue Drugs – Together

    Help Cure Muscular Dystrophy

    Help Fight Childhood Cancer

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  • richardmitnick 8:47 am on October 5, 2015 Permalink | Reply
    Tags: , , , Medicine, Pegivirus   

    From COSMOS: “The virus that could help stop HIV” 

    Cosmos Magazine bloc


    5 Oct 2015
    Viviane Richter

    Researchers are starting to unravel the secrets of a virus that not only doesn’t make you sick, but can help you fight off other diseases.

    Macaque monkeys can become infected with the primate version of the pegivirus Credit: egortupikov/gettyimages

    We’ve all heard of friendly bacteria, but a friendly virus? Called the pegivirus, catching it doesn’t make you sick. Instead, it can help the immune system to keep HIV infections in check. Discovered in 1995, scientists do not understand how it works, but that could soon change. Researchers at the Wisconsin National Primate Research Centre recently discovered baboons have their own pegivirus strain, offering a new way to study the oddball virus. Their investigation, published in Science Translational Medicine in September, may inspire new ways to tackle HIV.

    The pegivirus is found in about one in every six people, with infections lasting up to a decade before being cleared from the body. It can be transmitted from mother to child, through contact with an infected person’s blood, or sexually. In the US, where the virus is not included in routine blood bank screens, an estimated 1,000 people receive pegivirus-positive blood or blood products each day.

    While the pegivirus is genetically related to the hepatitis C virus, it doesn’t cause disease. On the contrary, researchers discovered in 2001 that the pegivirus appeared to protect some HIV-positive patients from developing AIDS. An 11-year study of 362 patients found 56% of HIV-positive people who did not carry pegivirus died. But among those patients infected with the pegivirus, the death rate was only 29%.

    How pegivirus thwarts HIV “has really been a bit confusing”, says Stephen Kent, an immunologist at the University of Melbourne. “But if you could mimic that with something that’s more potent – that would be good.”

    So what’s the pegivirus’ secret? “That’s the million-dollar question,” says Adam Bailey, lead author of the new study. Researchers need to study the pegivirus in an animal before it can be answered – one where the virus behaves much as it does in humans, happily cohabiting with its host without causing disease. Macaques failed the test: after being given human pegivirus they quickly cleared the infection. Maybe it was a matter of finding a money-version of the virus? Primates are known to carry viruses closely related to those we carry. For instance many primate species carry a virus closely related to HIV, called Simian Immunodeficiency Virus (SIV)

    So Bailey’s team hunted for a pegivirus that had struck up a long-term relationship with a non-human primate. They found it in 30-year-old samples of baboon blood stashed in a colleague’s freezer. Although that virus was genetically similar to the human strain, when it was injected into macaques it stayed in their blood for up to 200 days without causing harm, long enough for the researchers to study it.

    The researchers euthanised some infected monkeys, analysed their tissues for pegivirus RNA, and found most of the virus nestled in the spleen and bone marrow. These are also the tissues where HIV holes up. Pegivirus appeared to be actively replicating only in bone marrow, since removing the spleen of an infected monkey did not change the blood levels of the virus.

    The fact that pegivirus and HIV are replicating in the same tissues – though not necessarily in the same cells – offers a further a clue to how pegivirus may thwart HIV, says the study’s senior author, David O’Connor.

    When the immune system detects an invading virus, it pumps out more T cells – the infantry of the immune army. Alas that strategy plays right into the enemy’s hands since HIV replicates in and destroys those very cells. More T cells are produced to make up the casualties, giving HIV more cells to exploit. This vicious cycle decimates the immune system.

    Cell infected with HIV. HIV attacks T cells, which are crucial in the body’s immune system. The pegivirus helps the body resist HIV.Credit: THOMAS DEERINCK / NCMIR / getty images

    The researchers found pegivirus seems to slow the recruitment of new T cells from bone marrow. Kent speculates the pegivirus might prompt T cells to make molecules that lock HIV out. For instance the anti-HIV drug Maraviroc acts this way by blocking the CCR5 receptor on T cells.

    The Wisconsin team’s next step will be to co-infect macaques with pegivirus and SIV, the monkey form of HIV, to see how the viruses interact. They hope that once they discover how the pegivirus blocks HIV, they’ll be able to mimic the action with a drug.

    Today’s antiretroviral drugs are good at keeping HIV at bay – it’s estimated they’ve lowered the number of HIV deaths by two-thirds. But as O’Connor says “there’s a lot of space to help people even further”

    See the full article here .

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  • richardmitnick 11:15 am on October 3, 2015 Permalink | Reply
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    From Oxford: “Behind the scenes of creating the ground-breaking Ebola vaccine” 

    U Oxford bloc

    Oxford University

    Professor Adrian Hill of Oxford’s Jenner Institute led the first clinical trial of a successful Ebola virus vaccine last year. To target the outbreak his remarkable team compressed a process that takes six months into six weeks.


    The recent Ebola outbreak was the deadliest since the virus’ discovery in the 1970s. Fortunately Professor Adrian Hill, Director of Oxford’s Jenner Institute, and his team managed to create a vaccine response in record time.

    At his Alumni Weekend talk, Professor Hill described the desperate situation that West Africa was in last year. Ebola was in the news every day, with death tolls spiralling up through the summer. There were no vaccines known to protect against Ebola, or drugs to treat those infected at the time. Promising vaccine candidates did exist in the US, but only one had been tested in humans and had been subsequently abandoned.

    Usually Ebola outbreaks have been contained using the traditional methods of containment in Central Africa, but it was spreading through the continent rapidly – in Guinea, Sierra Leone, and Liberia – in 2014. With no vaccines ready to be tested out in West Africa the situation was grave, Professor Hill explained.


    The resulting ambitious trial at Oxford was funded by the Wellcome Trust, Medical Research Council and Department for International Development. Phase one began in mid-September 2014 with 60 volunteers, and a further 80 out in Mali in October – after the team was swamped with volunteers anxious to help.

    For the successful vaccine Professor Hill’s team used a single Ebola gene in a chimpanzee adenovirus to generate an immune response. As it did not contain any infectious virus material, it did not cause the patient to become infected. The trial’s efficiency exceeded all expectations, with a novel vaccine ready from the trial to finished product in nine months.


    The researchers then used an innovative trial design in West Africa, in which the family, friends and contacts in a ‘ring’ around an Ebola patient would be given the vaccine. In March 2015, the first infected individuals were identified and the ring vaccination began in Guinea, which continues to have the majority of cases. Both this ‘ring’ approach and the vaccine were a great success.

    Looking to the future, Professor Hill reflected that it would be wonderful if Britain could manufacture vaccines ‘on a significant scale’ once again. David Cameron has promised £20million to protect Britain from future pandemics this year, but how that money will be allocated has not yet been decided.

    Professor Hill explained more broadly the challenges left facing vaccination development. On the positive side, only two countries in the world are left with polio, and smallpox has been eradicated. This leaves the big three vaccinations to find as HIV/AIDS, malaria, and an improved TB jab.

    In terms of Ebola itself, the vaccine that Professor Hill’s team worked on was for the Zaire strain, but there still remains to be one for the Sudan strain. He pointed out that there will ‘almost certainly’ be more major outbreaks, especially as Africa’s population increases, people travel more and cities expand.

    For all of the team’s hard work, the University decided that their contributions should be recognised, and commissioned a University of Oxford Ebola medal this summer. The medals were presented by the Vice-Chancellor, Professor Andrew Hamilton, and the head of the Nuffield Department of Clinical Medicine, Professor Peter Ratcliffe. Professor Hamilton reflected: ‘The work of the team was absolutely critical. These kinds of outbreaks can arise at any time and we need to be ready to respond. They responded magnificently.’

    For further details about the Jenner Institute click here.

    Photographs courtesy of Oxford University Images

    See the full article here.

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    U Oxford campus

    Oxford is a collegiate university, consisting of the central University and colleges. The central University is composed of academic departments and research centres, administrative departments, libraries and museums. The 38 colleges are self-governing and financially independent institutions, which are related to the central University in a federal system. There are also six permanent private halls, which were founded by different Christian denominations and which still retain their Christian character.

    The different roles of the colleges and the University have evolved over time.

  • richardmitnick 9:36 am on October 3, 2015 Permalink | Reply
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    From Wyss Institute at Harvard: “How stem-cell research has received a boost” 

    Harvard University

    Harvard University

    Harvard Wyss Institute
    Wyss Institute

    Sep 18 2015
    Benjamin Boettner
    Kat J. McAlpine


    Possible stem cell therapies often are limited by low survival of transplanted stem cells and the lack of precise control over their differentiation into the cell types needed to repair or replace injured tissues. A team led by David Mooney, a core faculty member at Harvard’s Wyss Institute, has now developed a strategy that has experimentally improved bone repair by boosting the survival rate of transplanted stem cells and influencing their cell differentiation. The method embeds stem cells into porous, transplantable hydrogels.

    In addition to Mooney, the team included Georg Duda, a Wyss associate faculty member and director of the Julius Wolff Institute for Biomechanics and Musculoskeletal Regeneration at Charité – Universitätsmedizin in Berlin, and Wyss Institute founding director Donald Ingber. The team published its findings in today’s issue of Nature Materials. Mooney is also the Robert P. Pinkas Family Professor of Bioengineering at the Harvard John A. Paulson School of Engineering and Applied Sciences.

    Stem cell therapies have potential for repairing many tissues and bones, or even for replacing organs. Tissue-specific stem cells can now be generated in the laboratory. However, no matter how well they grow in the lab, stem cells must survive and function properly after transplantation. Getting them to do so has been a major challenge for researchers.

    Mooney’s team and other researchers have identified specific chemical and physical cues from the stem cell niche (the area in which stem cells survive and thrive with support from other cell types and environmental factors) to promote stem cell survival, multiplication and maturation into tissue. Whereas chemical signals that control stem cell behavior are increasingly understood, much less is known about the mechanical properties of stem cell niches. Stem cells like those present in bone, cartilage, or muscle cultured in laboratories, however, have been found to possess mechanosensitivities, meaning they require a physical substrate with defined elasticity and stiffness to proliferate and mature.

    “So far these physical influences had not been efficiently harnessed to propel real-world regeneration processes,” said Nathaniel Huebsch, a graduate student who worked with Mooney and who is the study’s first author. “Based on our experience with mechanosensitive stem cells, we hypothesized that hydrogels could be leveraged to generate the right chemical and mechanical cues in a first model of bone regeneration.”

    Two water-filled hydrogels with very different properties are the key to the Mooney team’s method. A more stable, longer-lasting “bulk gel” is filled with small bubbles of a second, so-called “porogen” that degrades at a much faster rate, leaving behind porous cavities.

    By coupling the bulk gel with a small “peptide” derived from the extracellular environment of genuine stem cell niches, and mixing it with a tissue-specific stem cell type as well as the porogen, the team can create a bone-forming artificial niche. While the bulk gel provides just the right amount of elasticity plus a relevant chemical signal to coax stem cells to proliferate and mature, the porogen gradually breaks down, leaving open spaces into which the stem cells expand before they naturally migrate out of the gel structure altogether to form actual mineralized bone tissue.

    In small-animal experiments conducted so far, the researchers show that a void-forming hydrogel with the correct chemical and elastic properties provides better bone regeneration than transplanting stem cells alone. Of further interest, the maturing stem cells deployed by the hydrogel also induce nearby native stem cells to contribute to bone repair, further amplifying their regenerative effects.

    “This study provides the first demonstration that the physical properties of a biomaterial can not only help deliver stem cells but also tune their behavior in vivo,” said Mooney. “While so far we have focused on orchestrating bone formation, we believe that our hydrogel concept can be broadly applied to other regenerative processes as well.”

    The collaborative, cross-disciplinary work was supported by the Harvard University Materials Research Science and Engineering Center (MRSEC), which is funded by the National Science Foundation (NSF).

    “This is an exquisite demonstration of MRSEC programs’ high impact,” said Dan Finotello, program director at the NSF. “MRSECs bring together several researchers of varied experience and complementary expertise who are then able to advance science at a considerably faster rate.”

    Additional funding was provided by the National Institutes of Health; the Belgian American Education Foundation; the Einstein Foundation Berlin; the Berlin-Brandenburg School for Regenerative Therapies; the Harvard College Research Program; and NSF Graduate Research, Einstein Visiting, Harvard College PRISE, Herchel-Smith and Pechet Family Fund Fellowships.

    See the full article here .

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    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

  • richardmitnick 2:53 pm on September 28, 2015 Permalink | Reply
    Tags: , Medicine,   

    From TUM: “25 million euros for multiple sclerosis research” 

    Techniche Universitat Munchen

    Techniche Universitat Munchen

    Dr. Vera Siegler

    On September 23, representatives of TUM and Klaus Tschira Foundation signed the contract for the new research center (f.l.t.r.): Harald Tschira and Beate Spiegel, Directors of the Klaus Tschira Foundation, Prof. Wolfgang A. Herrmann, President of TUM (Photo: A. Eckert / TUM)

    As one of the central fields of medical research at the Technical University of Munich (TUM), neuroscience is to gain a new research center for multiple sclerosis (MS). In Germany alone, some 200,000 people are affected by this as yet incurable disease, the cause of which remains unknown. Researchers at the TUM Klinikum rechts der Isar will now focus on MS and link clinical aspects of the disease with basic research. This major project has been enabled thanks to a 25 million euro donation by the Klaus Tschira Foundation, established by physicist Klaus Tschira. The associated contract was signed today by the President of TUM, Prof. Wolfgang A. Herrmann, and Directors of the Klaus Tschira Foundation, Beate Spiegel and Harald Tschira.

    In multiple sclerosis, the most common inflammatory disease of the central nervous system, the protective outer coating of the nerves is attacked and destroyed by the body’s own immune system, for reasons that are as yet unknown. The loss of this protective coating results in damage to the nerve fibers of the brain and spinal cord. Symptoms range from sensations of numbness to visual disorders, loss of coordination, problems with concentration and even paralysis.

    Each year, 1000 MS patients receive treatment at TUM Klinikum rechts der Isar, and numerous research groups there study the disease. The Klaus Tschira Foundation’s comprehensive financial support will now be used to establish a new MS treatment and research center within the grounds of the university hospital.

    “We are convinced that bringing outstanding scientists together in this new center will make a vital contribution to advancing research into the causes and treatment of MS”, say Harald Tschira and Beate Spiegel in relation to the Klaus Tschira Foundation’s involvement. “Of the 25 million euros, 20 million are for construction and 5 million for research.”

    TUM President Herrmann is very pleased: “The new research center will be a great success, and we thank the Klaus Tschira Foundation for it. The new build will give the excellent scientists already working at the Technical University of Munich a shared address right in the middle of the medical campus of TUM Klinikum rechts der Isar. This generous donation substantiates our reputation in neuroscience, recently boosted once more by the appointment of top researcher Prof. Mikael Simons from Göttingen.”

    Building on existing: MS research at TUM

    The main effect of the new build will be to bring the existing MS-related research groups at TUM together under a single roof. Scientists working on basic research and clinical research will work closely together to ensure that new discoveries are quickly translated into practical applications. As well as studying the immune system, scientists in the new research center will investigate the mechanisms that trigger damage to the nerve coatings and to the nerve fibers themselves. Their findings will feed into new therapeutic approaches, targeting especially the progressive stage of the disease.

    “This research center will be unique in Germany, with doctors and scientists in areas ranging from clinical practice to basic research working together under a single roof”, says Prof. Bernhard Hemmer, Director of the Department of Neurology, TUM Klinikum rechts der Isar. “MS patients will be the main beneficiaries of this new structure, since the systematic utilization of research results extends the range of treatment options and will one day enable individualized treatment of the disease.”

    See the full article here .

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    Techniche Universitat Munchin Campus

    Technische Universität München (TUM) is one of Europe’s top universities. It is committed to excellence in research and teaching, interdisciplinary education and the active promotion of promising young scientists. The university also forges strong links with companies and scientific institutions across the world. TUM was one of the first universities in Germany to be named a University of Excellence. Moreover, TUM regularly ranks among the best European universities in international rankings.

  • richardmitnick 9:07 am on September 27, 2015 Permalink | Reply
    Tags: , , Medicine, Spinal muscular atrophy (SMA)   

    From Harvard: “Hope against disease targeting children” 

    Harvard University

    Harvard University

    September 24, 2015
    Hannah Robbins, HSCI Communications

    Researchers identify molecular changes in genetic ailment, see ties to ALS behavior

    Temp 1
    In the right-hand picture, an SMA mouse treated with guanabenz, a compound known to reduce cellular stress, shows healthy junctions between muscle cells (red) and motor nerve fibers (green). In contrast, the untreated SMA mouse (left) has lost its nerve fibers, leaving the muscle cells with no way to receive signals from neurons in the spinal cord. Photo courtesy of Shi-Yan Ng

    Harvard Stem Cell Institute (HSCI) researchers studying spinal muscular atrophy (SMA) have found what they term “surprising similarities” between this childhood disorder that attacks motor neurons and amyotrophic lateral sclerosis (ALS), more commonly known as Lou Gehrig’s disease.

    The findings have been published online by the journal Cell Stem Cell.

    The research team led by HSCI principal faculty member Lee Rubin uncovered molecular changes that explain, at least in part, why motor neurons rather than others are affected by the illness. Unlike ALS and other neurodegenerative diseases, which tend to manifest later in life, SMA strikes infants. Unlike ALS, SMA is a genetic disorder that causes a range of outcomes, with the milder form leaving some children confined to wheelchairs, and the more severe form causing paralysis and death before the second birthday.

    Though not as well-known as ALS, SMA is “the most frequent fatal genetic disease of young children,” said Rubin, a professor in Harvard’s Department of Stem Cell and Regenerative Biology (HSCRB). About one in 50 people are carriers of SMA and about one in 5,000 children are born with the disease.

    Rubin said researchers are still working to determine the mechanisms of SMA. “It has never been clear why motor neurons — which relay signals from the brain to the muscles via the spinal column — die selectively,” Rubin said. “It is clear motor neurons die well before other kinds of cells, even other kinds of spinal-cord neurons, and the mystery has been trying to understand that.”

    A research team composed of HSCI investigators at the Broad Institute of Harvard and MIT and HSCRB, including HSCI principal faculty member John Rinn, worked in collaboration with the SMA Foundation’s Pediatric Neuromuscular Clinical Research Network and Wendy Chung from Columbia University College of Physicians and Surgeons to make neurons from donors with SMA of varying degrees of severity.

    The researchers first determined that the neurons in a dish behaved similarly to the way neurons would behave in an SMA patient. Not only did motor neurons die before other types of neurons, but motor neurons derived from patients with severe SMA died very quickly in comparison to those made from patients with a milder form of the disease.

    Then, using a method of intracellular cell labeling developed in HSCI co-director Doug Melton’s lab, the researchers separated motor neurons from other types of neurons in the dish, carried out an RNA sequencing analysis, and compared SMA motor neurons to those from healthy individuals.

    Healthy cells have mechanisms that help maintain an appropriate quantity of protein made by genes that are turned on within a given cell. There is a balance between protein production and protein degradation. Over time, neural cells targeted by late-onset neurodegenerative diseases — Parkinson’s, Alzheimer’s, Huntington’s, even ALS — lose their ability to maintain that balance. Proteins build up, and the clutter stresses the cell. If cells cannot resolve the issue, they shut down and die. After a number of cells have died, patients start to experience the effects of their disease.

    SMA, however, appears to work in the opposite way. There isn’t too much but too little of a specific protein, called survival of motor neuron (SMN), because the gene that codes that protein is broken. The researchers learned that a reduction in this protein affects the cells’ ability to process other proteins normally, leading to a motor neuron stress response. In particular, reduction in SMN causes a reduction in the levels of a chaperone protein that, Rubin said, acts like a protein traffic guard inside motor neurons. When other proteins are not folding correctly, the chaperone will hold up the stop sign, giving the other protein time to fold correctly before moving through the rest of the cell. If there are too few functional chaperones, it causes a protein traffic jam inside the cell. The buildup of these other proteins activates a stress response.

    When the research team shut off the stress response in the SMA-affected cells, both in culture and in a mouse model, they were able to keep the motor neuron cells from dying. “You could say that ALS and SMA converge on a pathway that causes motor neurons to be stressed,” Rubin said.

    Even though the two diseases have different origins — one with too much of the disease protein in the cells and the other with too little­­ — the point of convergence may be important, said Rubin. Because they both involve a stress response in motor neurons specifically, it is possible that the two diseases could eventually be treated by one drug.

    See the full article here .

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    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

  • richardmitnick 4:15 pm on September 8, 2015 Permalink | Reply
    Tags: , Macular Degeneration, Medicine,   

    From Buffalo: “Vitamin D may play key role in preventing macular degeneration” 

    SUNY Buffalo

    SUNY Buffalo

    August 27, 2015
    David J. Hill
    Tel: 716-645-4651

    UB research shows women with two risk alleles and low D status are more likely to have the disease

    Amy Millen, associate professor of epidemiology and environmental health in the University at Buffalo’s School of Public Health and Health Professions, is lead author on a paper published Aug. 27 in JAMA Ophthalmology.

    Vitamin D has been studied extensively in relation to bone health as well as cancer. Now, a team led by a researcher at the University at Buffalo has discovered that vitamin D may play a significant role in eye health, specifically in the possible prevention of age-related macular degeneration, or AMD, among women who are more genetically prone to developing the sight-damaging disease.

    In a paper published today (Aug. 27) in JAMA Ophthalmology online, Amy Millen, associate professor of epidemiology and environmental health in UB’s School of Public Health and Health Professions, and her team found that women who are deficient in vitamin D and have a specific high-risk genotype are 6.7 times more likely to develop AMD than women with sufficient vitamin D status and no high risk genotype.

    “Most people have heard that you should eat carrots to help your vision. However, there appear to be many other ways that adequate nutrition can support eye health. Having adequate vitamin D status may be one of them,” says Millen, PhD, the study’s lead author. “This is not a study that can, alone, prove a causal association, but it does suggest that if you’re at high genetic risk for AMD, having a sufficient vitamin D status might help reduce your risk.”

    “To our knowledge, this is the first study that’s looked at the interaction between genetic risk and vitamin D status in the context of age-related eye disease,” adds Millen.

    Macular degeneration is characterized by the deterioration of the macula, a small part of the central retina where the eye’s photoreceptors (rods and cones) are most highly concentrated. The leading cause of legal blindness, macular degeneration affects more than 10 million Americans — more than cataracts and glaucoma combined — according to the American Macular Degeneration Foundation. The disease affects a person’s central vision, which is needed for common tasks such as reading and driving. The effect is similar to that of a rain drop on the center of a camera lens.

    Researchers analyzed data compiled on 1,230 women ages 54 to 74 who participated in the Carotenoids in Age-related Eye Disease Study (CAREDS), which is an ancillary study of the Women’s Health Initiative (WHI) Observational Study (OS). The WHI OS is a major National Institutes of Health-funded research program aimed at addressing the most common causes of death, disability and poor quality of life in postmenopausal women. UB is one of 40 WHI centers nationally. CAREDS was conducted among participants at three of the centers: University of Wisconsin (Madison), the University of Iowa (Iowa City) and the Kaiser Center for Health Research (Portland, Oregon).

    Researchers were able to determine participants’ vitamin D status by analyzing serum samples for a vitamin D biomarker, 25-hydroxyvitamin D [25(OH)D], which provided a glimpse into vitamin D intake through all sources: diet, supplements and sunlight.

    Human skin can synthesize vitamin D when exposed to ultraviolet light, Millen explains. However, for many people, 15 to 30 minutes a day with 10 percent of their skin exposed might be sufficient. In winter months, when there is a lower solar angle, sun exposure may not be not sufficient to maintain blood level for people who live north of a line from about Washington, D.C., to Los Angeles. At these times and locations, dietary intake may be needed. Dietary sources of vitamin D include fortified foods such as milk and foods that naturally contain vitamin D such as fatty fish like salmon and mackerel.

    “Macular degeneration has been found to be strongly associated with genetic risk,” Millen says. Among many genes linked to AMD, one of the strongest is a specific genetic variant (Y402H) in the complement factor H gene, called CFH for short. This gene codes for the CFH protein that is involved in the body’s immune response to destroy bacteria and viruses.

    Inflammation is believed to be involved in the development of macular degeneration.

    “People who have early stage AMD develop drusen, lipid and protein deposits that build up in the eye. Your body sees this drusen as a foreign substance and attacks it, in part via the complement cascade response,” explains Millen. “CFH is one of the proteins involved in this response. We see more AMD in people who have certain variants in the gene which encodes a form of this CFH protein that is associated with a more aggressive immune response.”

    Vitamin D shows promise for protecting against macular degeneration because of its anti-inflammatory and antiangiogenic properties; antiangiogenic refers to slowing the growth of new blood vessels, often seen in late stages of AMD.

    “Our thinking was, if a person’s vitamin D status is better, would it reduce the immune response to drusen? We wanted to understand if the association between vitamin D and AMD differed depending on a person’s genetic risk for AMD,” says Millen. “Our study suggests that being deficient for vitamin D may increase one’s risk for AMD, and that this increased risk may be most profound in those with the highest genetic risk for this specific variant in the CFH protein.”

    The study results, however, shouldn’t prompt people to run to the nearest grocery store to purchase vitamin D supplements.

    “Our message is not that achieving really high levels of vitamin D are good for the eye, but that having deficient vitamin D levels may be unhealthy for your eyes,” Millen says.

    Although the odds of having AMD was higher in women who were deficient for vitamin D, with 25(OH)D levels below 12 ng/mL (30 nmol/L), increasing vitamin D levels beyond 12 ng/mL did not further lower the odds of AMD to any meaningful extent, she explains.

    “This study supports a role for vitamin D in eye health. That’s significant because when the Institute of Medicine’s report on the dietary reference intakes for vitamin D and calcium were released in 2011, the committee could only make conclusions about D related to bone health,” says Millen. “There wasn’t enough evidence at that time to make any recommendation based on D status and other outcomes beyond bone health.”

    Millen’s co-authors on the paper, titled “Association between vitamin D status and age-related macular degeneration by genetic risk,” include researchers from the University of Wisconsin-Madison, University of Iowa, Case Western Reserve University, Kaiser Permanente Center for Health Research and Fred Hutchinson Cancer Research Center. The study was funded by the National Eye Institute of the National Institutes of Health.

    See the full article here .

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    SUNY Buffalo Campus

    UB is a premier, research-intensive public university and a member of the Association of American Universities. As the largest, most comprehensive institution in the 64-campus State University of New York system, our research, creative activity and people positively impact the world.

  • richardmitnick 9:29 am on September 8, 2015 Permalink | Reply
    Tags: , Medicine, , Plague   

    From NYT: “Plague Cases in U.S. on the Rise” 

    New York Times

    The New York Times

    September 7, 2015
    Nicholas Bakalar

    No image credit.

    There have been 13 cases and three deaths from plague in the United States in the past five months, but researchers do not know why the disease appears to be on the rise.

    The number of plague cases in the United States usually averages about three a year. The Centers for Disease Control and Prevention reported last week that the recent cases of plague have afflicted residents of Arizona, California, Colorado, Georgia, New Mexico, Oregon and Utah. Two cases have been linked to exposure in or near Yosemite National Park.

    While doctors say there is no need to panic, there are some practical precautions that outdoor adventurers should take, particularly if they are traveling in one of the affected states. Plague is usually spread by bites from rodents and the fleas that feed on them.

    Dr. Christina Nelson, a medical epidemiologist with the C.D.C. and an author of the report, said using insect repellents and wearing long pants were practical ways to prevent exposure.

    “If you do get a fever or lymph node swelling after being outdoors, make sure to see a health care provider and tell them where you’ve been,” she advises.

    There are three types of plague: bubonic, which affects the lymph nodes; septicemic, a blood infection; and the most contagious form, pneumonic, which infects the lungs. There have been no pneumonic cases, and no person-to-person transmissions.

    There is no vaccine for plague, but it can be treated and cured with antibiotics. Untreated, it is 66 to 93 percent fatal.

    See the full article here .

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  • richardmitnick 7:13 pm on September 7, 2015 Permalink | Reply
    Tags: , , Medicine   

    From Science Times: “Link Between Obesity and Alzheimer’s Discovered — Study” 

    Science Times

    Science Times

    Sep 07, 2015
    Darlene Tverdohleb

    (Photo : . Reuters/Edgard Garrido) A woman with an instructor perform squats at Rio de los Remedios metrobus station in Mexico City. To combat growing obesity, lawmakers have introduced a new campaign encouraging physical activity. New study links obesity in midlife with more risks of developing Alzheimer’s disease.

    A new research study performed by scientists from the National Institutes of Health reveals that midlife obesity can lead to developing Alzheimer’s disease, and may also instigate an earlier onset of the illness.

    According to the study with a large prospective base, performed at the National Institute on Aging, excess weight around middle age could also increase the risk for amyloid deposits and neurofibrillary tangles in the brain. According to specialists, Alzheimer’s starts ravaging the brain quietly more than a decade before the first symptoms appear.

    From the participants in the study, during the follow-up phase, 142 of the them have developed the disease. Researchers have been trying to find some ways to delay the outset of the disease and it seems that a change in human lifestyle could be a possible option.

    Dr. Madhav Thambisetty of National Institute on Aging, the expert who led the survey, explained that even though other field experts are aware of the fact that overweight people or people who are obese during their midlife years could be more vulnerable to developing Alzheimer’s disease, they still cannot explain “how it may affect the age when the disease first begins.”

    Thambisetty said that by maintaining a healthy weight at midlife people are likely to gain a long-lasting protective effect. The research team studied how much those Alzheimer’s patients weighed at the age of 50 while they were still cognitively healthy. The study findings suggest that, in average, Alzheimer’s set in about seven months earlier for each unit increase in body mass index (BMI).

    Men and women participating in the study had at 50 years an average BMI of 25.7. The researchers concluded that losing weight would decelerate the rate of onset. However, not all the overweight participants in the study developed the Alzheimer’s disease. Also, the Alzheimer’s study didn’t track the fluctuations in patients’ BMI before or after age 50, so more following studies might find more insights into the link between BMI and Alzheimer’s.

    Some of the participants in the Baltimore Longitudinal study underwent brain scans during life and autopsies at death. However, despite this alarming link between obesity and Alzheimer’s, health researchers have yet to identify the elements that cause the illness to develop.

    See the full article here .

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    We provide credible news & info., in-depth reference material about diverse subjects that matter to everyone. We are a source for original and timely science and research information as well as breaking news in the various fields we represent.

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