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  • richardmitnick 9:42 am on April 23, 2016 Permalink | Reply
    Tags: , , , Medicine,   

    From WIRED:”Technology Aids in Fight Against Tuberculosis” 

    Discovery News
    Discovery News

    For the first time ever, a supercomputer will help in the fight against one of the deadliest and fastest-spreading diseases in the world: tuberculosis.

    2

    1

    In one corner of the ring you have the IBM World Community Grid.

    WCG Logo New

    WCGLarge

    This platform gives anyone a chance to join the fight by donating their devices’ spare energy. This means they can use the energy from your computer, tablet or smartphone when your device is idle. The World Community Grid is one the most powerful platforms on the planet, and its newly launched Help Stop TB project is fantastic news for the medical community. In the other corner, we have tuberculosis.

    What Is Tuberculosis?

    Tuberculosis is a highly contagious, airborne disease that kills about 1.5 million people each year. A tuberculosis infection can begin without any symptoms and can persist for years before it becomes an active disease. If TB is detected early, then it is easily treatable. It’s important to look for symptoms and seek treatment.

    Active tuberculosis is contagious and spread through the air. Sneezing, coughing or talking is all it takes to spread the disease to another person. Anyone can easily catch this disease. This is why it’s important to find a cure as soon as possible, and IBM’s technology can certainly help in a major way.

    The Advantages of Technology

    The World Community Grid is no stranger to medical advances. Since its creation in 2014, the World Community Grid has contributed to research for many causes like curing AIDS, cancer and world hunger.

    With about 700,000 people lending their devices’ energy to IBM, the World Community Grid is a top-10 supercomputer.

    IBM

    SmarterPlanet

    This makes the research process much more efficient. Researchers can now categorize and go through data at rapid speeds.

    When it comes to medical research, the more technology the better. Scientists have been using cloud capabilities to apply tens of thousands of computer nodes to a single problem. Supercomputers offer a way to quickly scan through and recognize problems that may have taken years to uncover.

    A team at Novartis was able to run through 40 years of cancer drug simulations in just eight hours. It also cost them thousands of dollars instead of the millions it would’ve cost before supercomputers. Having a supercomputer that uses the energy from the devices of 700,000 people will only help tuberculosis research.

    The Fight Against Tuberculosis

    Tuberculosis is coined as the world’s deadliest disease, so it’s vital that scientists find a cure as soon as possible. It received this nickname because it kills about 1.5 million people a year. IBM’s World Community Grid supercomputer will tremendously speed up the process.

    Scientists will use the World Community Grid to get a complete understanding of TB’s cell wall. They’ll be able to simulate different variations of mycolic acid structures to see if they can impact the bacteria’s functions. The supercomputer lets them test many different structures instead of just a few. They hope that one of these structures will give scientists a better understanding of how to attack tuberculosis.

    You Can Help

    You can sign up to let IBM use your devices’ energy when you aren’t using them. Sign up today and be a part of the fight against tuberculosis.

    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.

    BOINC WallPaper

    CAN ONE PERSON MAKE A DIFFERENCE? YOU BET!

    “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.

    Please visit the project pages-
    Outsmart Ebola together

    Outsmart Ebola Together

    Mapping Cancer Markers
    mappingcancermarkers2

    Uncovering Genome Mysteries
    Uncovering Genome Mysteries

    Say No to Schistosoma

    GO Fight Against Malaria

    Drug Search for Leishmaniasis

    Computing for Clean Water

    The Clean Energy Project

    Discovering Dengue Drugs – Together

    Help Cure Muscular Dystrophy

    Help Fight Childhood Cancer

    Help Conquer Cancer

    Human Proteome Folding

    FightAIDS@Home

    World Community Grid is a social initiative of IBM Corporation
    IBM Corporation
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    IBM – Smarter Planet
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    See the full article here .

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  • richardmitnick 10:40 am on April 1, 2016 Permalink | Reply
    Tags: , , , Medicine   

    From AAAS: “Alzheimer’s may be caused by haywire immune system eating brain connections” 

    AAAS

    AAAS

    Mar. 31, 2016
    Emily Underwood

    1
    Over-pruning synapses may drive early-stage Alzheimer’s disease. Eraxion/iStockphoto

    More than 99% of clinical trials for Alzheimer’s drugs have failed, leading many to wonder whether pharmaceutical companies have gone after the wrong targets. Now, research in mice points to a potential new target: a developmental process gone awry, which causes some immune cells to feast on the connections between neurons.

    “It is beautiful new work,” which “brings into light what’s happening in the early stage of the disease,” says Jonathan Kipnis, a neuroscientist at the University of Virginia School of Medicine in Charlottesville.

    Most new Alzheimer’s drugs aim to eliminate β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. Those with Alzheimer’s tend to have more of these deposits in their brains than do healthy people, yet more plaques don’t always mean more severe symptoms such as memory loss or poor attention, says Beth Stevens of Boston Children’s Hospital, who led the new work.

    What does track well with the cognitive decline seen in Alzheimer’s disease—at least in mice that carry genes that confer high risk for the condition in people—is a marked loss of synapses, particularly in brain regions key to memory, Stevens says. These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity.

    Stevens has spent much of her career studying a normal immune mechanism that prunes weak or unnecessary synapses as the brain matures from the womb through adolescence, allowing more important connections to become stronger. In this process, a protein called C1q sets off a series of chemical reactions that ultimately mark a synapse for destruction. After a synapse has been “tagged,” immune cells called microglia—the brain’s trash disposal service—know to “eat” it, Stevens says. When this system goes awry during the brain’s development, whether in the womb or later during childhood and into the teen years, it may lead to psychiatric disorders such as schizophrenia, she says.

    Stevens hypothesized that the same mechanism goes awry in early Alzheimer’s disease, leading to the destruction of good synapses and ultimately to cognitive impairment. Using two Alzheimer’s mouse models—each of which produces excess amounts of the β amyloid protein, and develops memory and learning impairments as they age—she and her team found that both strains had elevated levels of C1q in brain tissue. When they used an antibody to block C1q from setting off the microglial feast, however, synapse loss did not occur, the team reports today in Science.

    To Stevens, that suggests that the normal mechanism for pruning synapses during development somehow gets turned back on again in the adult brain in Alzheimer’s, with dangerous consequences. “Instead of nicely whittling away [at synapses], microglia are eating when they’re not supposed to,” she says.

    The group is now tracking these mice to see whether a drug that blocks C1q slows their cognitive decline. To determine whether elevated β amyloid can cause the C1q system to go haywire, Stevens and colleagues also injected a form of the protein which is known to generate plaques into the brains of normal mice and so-called knockouts that could not produce C1q because of a genetic mutation. Although normal mice exposed to the protein lost many synapses, knockouts were largely unaffected, Stevens says. In addition, microglia only went after synapses when β amyloid was present, suggesting that the combination of protein and C1q is what destroys synapses, rather than either element alone, she says, adding that other triggers, such as inflammatory molecules called cytokines, might also set the system off.

    The findings contradict earlier theories which held that increased microglia and C1q activity were merely part of an inflammatory reaction to β amyloid plaques. Instead, microglia seem to start gorging on synapses long before plaques form, Stevens says. She and several co-authors are shareholders in Annexon Biosciences, a biotechnology company that will soon start testing the safety of a human form of the antibody the team used to block C1q, known as ANX-005, in people.

    Such a central role for microglia in Alzheimer’s disease is “still on the controversial side,” says Edward Ruthazer, a neuroscientist at the Montreal Neurological Institute and Hospital in Canada. One “really compelling” sign that the mechanism is important in people would be if high levels of C1q in cerebrospinal fluid early on predicted developing full-blown Alzheimer’s later in life, he says. Still, he says, “it’s difficult to argue with the strength of the study’s evidence.”

    The science team:
    Soyon Hong1, Victoria F. Beja-Glasser1,*, Bianca M. Nfonoyim1,*, Arnaud Frouin1, Shaomin Li2, Saranya Ramakrishnan1, Katherine M. Merry1, Qiaoqiao Shi2, Arnon Rosenthal3,4,5, Ben A. Barres6, Cynthia A. Lemere,2, Dennis J. Selkoe2,7, Beth Stevens1,8,†

    Author Affiliations

    1F.M. Kirby Neurobiology Center, Boston Children’s Hospital and Harvard Medical School, Boston, MA 02115, USA.
    2Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA.
    3Alector Inc., 953 Indiana Street, San Francisco, CA 94107, USA.
    4Annexon Biosciences, 280 Utah Avenue Suite 110, South San Francisco, CA 94080, USA.
    5Department of Anatomy, University of California San Francisco, CA 94143, USA.
    6Department of Neurobiology, Stanford University School of Medicine, Palo Alto, CA 94305, USA.
    7Prothena Biosciences, Dublin, Ireland.
    8Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.

    ↵†Corresponding author. E-mail: beth.stevens@childrens.harvard.edu

    ↵* These authors contributed equally to this work.

    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 10:11 am on April 1, 2016 Permalink | Reply
    Tags: , Medicine, , Stroke   

    From SA: “A Hidden Factor in Stroke Severity: The Microbes in Your Gut” 

    Scientific American

    Scientific American

    March 30, 2016
    Jordana Cepelewicz

    1
    Micrograph showing cortical pseudolaminar necrosis, a finding seen in strokes on medical imaging and at autopsy. Nephron/Wikimedia Commons, CC BY-SA 3.0

    The bacteria that inhabit our guts have become key players for neuroscientists. A growing body of research links them to a wide array of mental and neurological disorders—from anxiety and depression to schizophrenia and Alzheimer’s disease. Now a study in mice published this week in Nature Medicine suggests that striking the right microbial balance could cause changes in the immune system that significantly reduce brain damage after a stroke—the second leading cause of both death and disability for people around the globe. (Scientific American is part of Springer Nature.)

    Experts have known for some time that stroke severity is influenced by the presence of two types of cell, found abundantly within the intestine, that calibrate immune responses: Regulatory T cells have a beneficial inflammatory effect, protecting an individual from stroke. But gamma delta T cells produce a cytokine that causes harmful inflammation after a stroke.

    A team of researchers at Weill Cornell Medical College and Memorial Sloan Kettering Cancer Center set about investigating whether they could tilt the balance of these cells in the favor of beneficial cells by tinkering with the body’s bacterial residents. To do so, they bred two colonies of mice: One group’s intestinal flora was resistant to antibiotics whereas the other’s gut bacteria was vulnerable to treatment. As a result, when given a combination of antibiotics over the course of two weeks, only the latter’s microbiota underwent change. The researchers then obstructed the cerebral arteries of the mice, inducing an ischemic stroke (the most common type). They found that subsequent brain damage was 60 percent smaller in the drug-susceptible mice than it was in the other group.

    To confirm that this result could truly be attributed to the change in intestinal flora, the researchers performed fecal transplants. That is, they took the contents of the colons of mice that had experienced reduced stroke and gave this material to new mice. This time, however, the team did not administer antibiotics, thus creating a group of mice with altered gut bacteria but no drug exposure. By inducing an ischemic attack in this group, the researchers discovered that these mice had also acquired protection against stroke.

    The researchers found that by altering intestinal flora they had indirectly pushed the ratio between immune cells in favor of the “good” regulatory T cells while suppressing the more harmful gamma delta T cells. The team tracked both kinds of cells as they left the gut and traveled to the brain, where they settled on the meninges and, the researchers suspect, conditioned how the brain responded to the stroke. This so-called systemic inflammatory response—supported by T cells—can be beneficial, clearing the brain of dead cells, or debilitating, causing brain swelling and further damage. “These cells determine what kind of inflammatory immune response the brain is going to experience after stroke,” says neurologist Constantino Iadecola, director of the Brain and Mind Research Institute at Weill Cornell and one of the study’s authors. By changing the bacterial landscape of the gut, he explains, “immune cells end up helping out instead of contributing to the damage that occurs.”

    “Now the microbiome is another element in this equation—it’s not just diabetes, high blood pressure and obesity,” Iadecola notes. “There are also other factors which we need to know in order to tailor treatment.” The study suggests that such treatment may involve antibiotics, probiotics, dietary changes or other interventions that would change the gut’s microbiota to be supportive of regulatory T cells and reduce delta gamma T cells. For example, patients undergoing heart surgery, many of whom end up suffering a stroke, might go on a special preemptive diet, he says.

    Such interventions remain a long way off, however. A mouse’s microbiome is very different from that of a human; researchers will need clinical data. Right now they are working on identifying the specific bacteria involved in their findings as well as the molecular mechanism—how exactly the gut and brain interact and communicate—that underlies the immune responses observed in this study. Both avenues of research are important for developing targeted therapeutic approaches down the line. “This is just the beginning,” says Ulrich Dirnagl, a neurologist at the Center for Stroke Research Berlin who did not participate in this research. “The study links the microbiota and the immune system and the brain in stroke—an acute brain disorder—in one story. That’s really novel. But this is not a therapy.” He adds, “In a different future you could argue that maybe what this means is there are certain kinds of microbiota that make humans more susceptible to having larger or smaller strokes. But saying that now would be premature.”

    Studying the link between intestinal composition and stroke risk would be a very complicated endeavor, as the human microbiome is influenced by a huge range of factors, including diet, living conditions and antibiotics. Still, the researchers are optimistic. “This emphasis on the microbiome, and sequencing it, is a young field,” says Weill Cornell neuroscientist and study author Josef Anrather. “Obviously it takes time. But the implications are there.”

    The science team:
    Corinne Benakis, David Brea, Silvia Caballero, Giuseppe Faraco, Jamie Moore, Michelle Murphy, Giulia Sita, Gianfranco Racchumi, Lilan Ling, Eric G Pamer, Costantino Iadecola & Josef Anrather

    Affiliations:

    Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, New York, USA.
    Corinne Benakis, David Brea, Giuseppe Faraco, Jamie Moore, Michelle Murphy, Giulia Sita, Gianfranco Racchumi, Costantino Iadecola & Josef Anrather
    Immunology Program and Infectious Disease Service, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
    Silvia Caballero & Eric G Pamer
    Immunology and Microbial Pathogenesis Program, Weill Cornell Graduate School of Medical Sciences, New York, New York, USA.
    Silvia Caballero & Eric G Pamer
    Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
    Lilan Ling & Eric G Pamer

    See the full article here .

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    Scientific American, the oldest continuously published magazine in the U.S., has been bringing its readers unique insights about developments in science and technology for more than 160 years.

     
  • richardmitnick 8:20 am on March 31, 2016 Permalink | Reply
    Tags: , , , Medicine   

    From AAAS: “Cause of rare immune disease identified” 

    AAAS

    AAAS

    Mar. 30, 2016
    Mitch Leslie

    1
    A newly discovered disease found in a Belgian family may cause illness by inappropriately activating the inflammasome, a cellular structure that triggers inflammation. Chris Bickel/Science

    The Belgian family had puzzled doctors for more than a decade. Beginning when they were children, some members were prone to bouts of fever that could last for months. Their muscles and joints ached, their blood vessels were inflamed, and their skin erupted with sores that ranged from severe acne to abscesses and ulcers. One patient’s heart was so badly damaged that he needed a transplant at the age of 20.

    Now, researchers have figured out why the family members became ill, revealing that they suffer from a previously undiscovered genetic disease that unleashes a protein that normally helps protect us from microbes. Armed with the findings, doctors might be able to recognize other people with similar symptoms who have gone undiagnosed and offer treatment. In addition, the researchers say, the results might provide insight into more common diseases such as inflammatory bowel disease, where inflammation is out of control.

    “The paper beautifully works out the biochemistry” of how the mutation that causes the new disease alters a key immune protein, says geneticist Daniel Kastner of the National Human Genome Research Institute in Bethesda, Maryland, who wasn’t connected to the research.

    Scientists have already identified several rare but painful diseases in which the immune system triggers inappropriate inflammation in various parts of the body. These conditions differ from autoimmune diseases like rheumatoid arthritis and type I diabetes because a different branch of the immune system, which includes the body’s first responders to foreign invaders, malfunctions. Some of the Belgian family’s symptoms resembled the symptoms of one of these so-called autoinflammatory diseases, familial Mediterranean fever (FMF), but they were much worse. In FMF, for instance, fever lasts for a few days, not months.

    FMF results from mutations in the gene for pyrin, a protein inside many immune cells that detects infections by certain microbes. One attempt to track down the genetic flaw in the Belgian sufferers suggested that they could carry a defect in the same gene, but researchers dismissed the possibility because their symptoms were so different from those in people with FMF, says immunologist Seth Masters of the Walter and Eliza Hall Institute of Medical Research in Parkville, Australia, a co-author on the new paper. “It really didn’t look like the same disease.”

    Yet when Masters and colleagues sequenced the DNA of the Belgian family, they found a mutation in the gene for pyrin. It’s in a different location than in most people with FMF, the team reports today in Science Translational Medicine. After searching disease databases and hearing from other doctors who had patients with the similar symptoms, the researchers identified three other families in Lebanon, France, and the United Kingdom that had the same mutation. They’ve named the resulting disease pyrin-associated autoinflammation with neutrophilic dermatosis (PAAND).

    Although the same gene is mutated in people with FMF, the type and severity of the symptoms confirm that PAAND is a unique disease, Kastner says. “It’s not FMF. Period.” It’s rare for different mutations in the same gene to cause distinct diseases, but PAAND and FMF are not the only examples, says medical geneticist Wayne Grody of the University of California, Los Angeles (UCLA), who wasn’t connected to the study. He notes, for instance, that mutations in the CFTR gene can trigger the potentially lethal disease cystic fibrosis or a milder illness that results in male infertility.

    Masters and colleagues further determined how the mutation in PAAND patients causes pyrin to go awry. When pyrin senses toxins released by some kinds of bacteria, it spurs formation of a structure called the inflammasome that in turn triggers inflammation. To prevent pyrin from switching on prematurely, cells typically shield it with another protein until they are in trouble. But the scientists found that this shield falls off the version of pyrin that the Belgian family produced, resulting in an overactive molecule. “In effect you take away the brake,” says co-author Adrian Liston, an immunologist at the University of Leuven in Belgium.

    What makes the paper stand out, says Grody, is the team’s thorough investigation. “They really have a mechanism—we don’t have anything like that to explain FMF,” he says. The work also points to a potential treatment, a drug that blocks an inflammation-promoting molecule that was abundant in the patients. When the researchers treated one member of the Belgian family with the drug, “all the signs of disease disappeared within a couple of weeks,” Liston says. “It was really quite remarkable.” The scientists now plan to launch a clinical trial of the drug in more PAAND patients. Masters and Liston say that the results could also help researchers better understand the role of inflammation in non–auto-inflammatory illnesses, including Alzheimer’s disease and inflammatory bowel disease.

    The study might provide more immediate benefits for some people as well. FMF is relatively common for an autoinflammatory disease, but even in the Mediterranean region only about one in 200 to one in 1000 people suffer from it. Although PAAND isn’t likely to be prevalent, researchers think that more patients are waiting for a diagnosis. Large numbers of people with the disease could live in populous countries such as India and China, Masters says. Grody and his colleagues at the FMF clinic at UCLA will be on the lookout for new cases. “I’m certain there are other families out there,” he says.

    Research Article
    Inflammation

    Familial autoinflammation with neutrophilic dermatosis reveals a regulatory mechanism of pyrin activation

    Science team:

    Seth L. Masters1,2,*, Vasiliki Lagou3,4,5,†, Isabelle Jéru6,7,8,†, Paul J. Baker1,2,†, Lien Van Eyck4,5, David A. Parry9, Dylan Lawless10, Dominic De Nardo1,2, Josselyn E. Garcia-Perez4,5, Laura F. Dagley1,2,11, Caroline L. Holley12, James Dooley4,5, Fiona Moghaddas1,2, Emanuela Pasciuto4,5, Pierre-Yves Jeandel13, Raf Sciot14,15, Dena Lyras16, Andrew I. Webb2,11, Sandra E. Nicholson1,2, Lien De Somer15, Erika van Nieuwenhove4,5,15, Julia Ruuth-Praz7,8, Bruno Copin8, Emmanuelle Cochet8, Myrna Medlej-Hashim17, Andre Megarbane18, Kate Schroder12, Sinisa Savic19,20, An Goris3, Serge Amselem6,7,8, Carine Wouters4,15,*,‡ and Adrian Liston4,5,*,‡

    Affiliations:

    1Inflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, 3052, Australia.
    2Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, Australia.
    3Department of Neurosciences, KU Leuven, Leuven 3000, Belgium.
    4Department of Microbiology and Immunology, KU Leuven, Leuven 3000, Belgium.
    5Translational Immunology Laboratory, VIB, Leuven 3000, Belgium.
    6INSERM, UMR S933, Paris F-75012, France.
    7Université Pierre et Marie Curie–Paris, UMR S933, Paris F-75012, France.
    8Assistance Publique Hôpitaux de Paris, Hôpital Trousseau, Service de Génétique et d’Embryologie médicales, Paris F-75012, France.
    9Centre for Genomic and Experimental Medicine, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road South, Edinburgh LS7 4SA, UK.
    10Leeds Institute of Biomedical and Clinical Sciences, University of Leeds, Wellcome Trust Brenner Building, Saint James’s University Hospital, Leeds LS7 4SA, UK.
    11Systems Biology and Personalised Medicine Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia.
    12Institute for Molecular Bioscience (IMB) and IMB Centre for Inflammation and Disease Research, The University of Queensland, Brisbane, Queensland 4072, Australia.
    13Département de Médecine Interne, Hôpital Archet 1, Université Nice Sophia-Antipolis, 06202 Nice, France.
    14Department of Pathology, KU Leuven, Leuven 3000, Belgium.
    15University Hospitals Leuven, Leuven 3000, Belgium.
    16Department of Microbiology, Monash University, Melbourne, Victoria 3800, Australia.
    17Department of Life and Earth Sciences, Faculty of Sciences II, Lebanese University, Beirut 1102 2801, Lebanon.
    18Al-Jawhara Center, Arabian Gulf University, Manama 26671, Bahrain.
    19Department of Allergy and Clinical Immunology, Saint James’s University Hospital, Leeds LS9 7TF, UK.
    20National Institute for Health Research–Leeds Musculoskeletal Biomedical Research Unit and Leeds Institute of Rheumatic and Musculoskeletal Medicine, Wellcome Trust Brenner Building, Saint James’s University Hospital, Beckett Street, Leeds LS9 7TF, UK.

    ↵*Corresponding author. E-mail: masters@wehi.edu.au (S.L.M.); carine.wouters@uzleuven.be (C.W.); adrian.liston@vib.be (A.L.)

    ↵† These authors contributed equally as second authors.

    ↵‡ These authors contributed equally as co-last authors.

    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 2:27 pm on March 30, 2016 Permalink | Reply
    Tags: , Help Stop TB, Medicine,   

    From The Conversation: “Tuberculosis kills thousands of people every day – we aren’t doing enough to stop it “ 

    Conversation
    The Conversation

    March 30, 2016
    Jane E. Hill, Associate Professor of Engineering, Dartmouth College

    1
    An x-ray showing a pair of lungs infected with TB (tuberculosis). Luke MacGregor/Reuters

    “But hasn’t TB been eradicated?,” my seatmate on a recent flight to South Africa asked me. This question crops up pretty frequently when I tell people what I do for a living. I research the development of diagnostic tests for diseases using breath, sputum, blood and urine, and at the moment I am working on a diagnostic breath test for tuberculosis.

    For most people in the West, TB seems to be a disease of the past, when it was still called consumption, and the ill were sent to sanitariums in the mountains or desert.

    But TB hasn’t gone away. In 2015 the number of TB cases in the U.S. rose for the first time in 23 years. In 2014 more than 500 people died from TB in the U.S. Even so, a lot of people have no idea that TB is still found here, or what a major health risk it poses in other parts of the world.

    My seatmate didn’t know, for instance, that South Africa has one of the highest incidence rates of TB in the world, and that disease had killed least 96,000 people there in 2015.

    Tuberculosis is an airborne killer

    In 2015, TB killed 1.5 million people worldwide, and an estimated 26,000 people are infected each day. Prevalence is highest in sub-Saharan Africa, from Ethiopia to South Africa, and in Asia, particularly in India and China.

    The disease is caused by Mycobacterium tuberculosis, an organism that has caused infection in humans since the stone age.

    And it’s airborne – aerosols containing the bacterium remain suspended in rooms for hours after being coughed out by a person with tuberculosis. Once inhaled, the mycobacterium has a very real chance of taking up residence in your lungs, where it can lead to one of two conditions: latent TB and TB disease.

    People with latent TB are infected, but don’t have symptoms and can’t transmit the disease. However, latent TB can transition to TB disease when a person’s immune system is suppressed, because of an HIV infection or malnutrition, for instance. In the West, people with latent TB are treated to prevent the infection from becoming active. About one-third of the world’s population has latent TB.

    TB disease, on the other hand, is infectious. The body’s response to the bacterium leads to a hypermetabolic state, draining nutrition from the body, leading to loss of weight or wasting. With your metabolism in overdrive, you become a skeletal vestige of yourself, waking up drenched in sweat each night.

    This is accompanied by a fight between the bacterium and immune system, which takes place in your lungs, leaving you with a persistent hacking cough that ends up producing a literal bloody mess.

    A person with TB disease is contagious for as long as they have TB symptoms. If untreated, it will probably kill you and could spread to people who live and work with you.

    2
    A tuberculosis patient ingests a medicine from a free treatment at a medical post in the outskirts of Lima in 2011. Enrique Castro-Mendivil/Reuters

    In the West, if a person is thought to have TB, skin and blood tests are usually the first diagnostic tests conducted, and if they generate a positive result, chest X-rays are taken, usually indicating that the patient has a latent infection. If the patient experiences night sweats, loss of weight and a persistent cough, then a sputum culture from the lung is sent off for testing. The sputum culture is the diagnostic “gold standard” used worldwide to confirm an active TB infection.

    Kids often have trouble producing sputum, so instead they inhale droplets of saline, which can help them cough up phlegm from their lower airway.

    Getting a result from a TB sputum culture test takes at least three weeks. Newer tests could decrease the time-to-result to a few hours, though in practice, the turnaround time is usually a few days. This time lag is one reason why up to 40 percent of patients who are tested never return to the clinic to learn the result.

    When a person is diagnosed with TB, they’ll begin treatment with antibiotics. The standard therapy is a daily cocktail of antibiotics for at least six months.

    While drug resistance in most countries hovers around a few percent of all TB cases reported (which is still noteworthy), some places, such as Russia, report that drug-resistant TB makes up a whopping rate of 19 percent of total cases.

    However, some strains of TB are becoming resistant to standard therapies. Globally an estimated 480,000 people developed drug-resistant TB in 2014. People infected with drug-resistant TB undergo a daily, painful injection plus daily oral, toxic drug cocktails for at least 18 months.

    Even with treatment, if you are infected with extremely drug-resistant TB, the risk of dying can be greater than 70 percent at five years after a full course or treatment, far worse than Ebola and most cancers.

    TB outbreaks are happening in the U.S.

    TB is still active in the U.S., and it is most likely to appear in large cities. New York and Los Angeles, for instance, are among cities that have seen recent outbreaks. These cities maintain at least marginal surveillance, in which people are screened for symptoms when they arrive from a destination where it is endemic. If they are infected, patients are placed onto supervised treatment.

    But TB outbreaks have also occurred well outside of major cities.

    Just last year Vermont had a mini-outbreak, in which eight people were infected at a rural K-8 school. In rural Alabama, an ongoing mini-outbreak has already killed three people and sickened over 70 others, with more new cases expected. While U.S. outbreaks have not yet been of the drug-resistant kind, we can’t assume that this luck will hold.

    3
    Patients with HIV and tuberculosis (TB) wear masks while awaiting consultation at a clinic in Cape Town’s Khayelitsha township, February 23, 2010. Finbarr O’Reilly/Reuters

    The World Health Organization has released a strategy to end the global TB epidemic by 2030. But the WHO estimates that there is a US$1.4 billion funding gap each year for treatment implementation. Research is also underfunded to the tune of $1.3 billion.

    To eliminate TB, we need better disease surveillance and monitoring in all countries, but especially locations where it is endemic, to help prevent outbreaks and get people into treatment. In addition, developing new diagnostics that can deliver results much faster and that don’t require laboratories is critical. And these tests need to work on adults and children.

    Making sure that TB patients get the support they need to comply with the months-long treatment regimen will also help. For those with multidrug-resistant TB, we need humane quarantine systems and a pipeline of non-toxic drugs so they have a reasonable chance of survival.

    If the number of people who still get infected with TB and the number of people who ultimately die from the disease are not impetus for us to pay more attention, surely the specter of a drug-resistant, airborne killer with a 70 percent death rate is a fate not worth tempting.

    See the full article here .

    Want to help end TB? Go to World Community Grid [WCG], download and install the BOINC software on which it runs, and attach to the very new TB Project, Help Stop TB.

    About the project:

    Proposed Solution
    The bacterium has an unusual coat which protects it from many drugs and the patient’s immune system. Among the fats, sugars and proteins in this coat, the TB bacterium contains a type of fatty molecules called mycolic acids. Help Stop TB will use the massive amount of computing power donated by World Community Grid members to simulate the behavior of these molecules in their many configurations to better understand how they offer protection to the TB bacteria. Scientists hope to use the resulting information to finally develop better treatments for this deadly disease.

    Help Stop TB

    WCG runs on BOINC software from UC Berkeley

    BOINC WallPaper

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    The Conversation US launched as a pilot project in October 2014. It is an independent source of news and views from the academic and research community, delivered direct to the public.
    Our team of professional editors work with university and research institute experts to unlock their knowledge for use by the wider public.
    Access to independent, high quality, authenticated, explanatory journalism underpins a functioning democracy. Our aim is to promote better understanding of current affairs and complex issues. And hopefully allow for a better quality of public discourse and conversation.

     
  • richardmitnick 9:25 am on March 30, 2016 Permalink | Reply
    Tags: , , GI tract bacteria helps decrease stroke severity, Medicine   

    From Cornell: “GI tract bacteria helps decrease stroke severity” 

    Cornell Bloc

    Cornell University

    March 28, 2016
    Abigail Fagan
    cunews@cornell.edu

    1
    Immune cells (green) assemble in the outer coverings of a mouse’s brain, called the meninges, protecting it from a stroke’s full force. Gut bacteria modified the immune’ cells behavior to elicit that protective response. Corinne Benakis

    Certain types of bacteria in the gut can leverage the immune system to decrease the severity of stroke, according to new research from Weill Cornell Medicine. This finding can help mitigate stroke, the second leading cause of death worldwide.

    In the study, published March 28 in Nature Medicine, mice received a combination of antibiotics. Two weeks later, the researcher team – which included collaborators at Memorial Sloan Kettering Cancer Center – induced the most common type of stroke, called ischemic stroke, in which an obstructed blood vessel prevents blood from reaching the brain. Mice treated with antibiotics experienced a stroke that was about 60 percent smaller than rodents that did not receive the medication. The microbial environment in the gut directed the immune cells there to protect the brain, the investigators said, shielding it from the stroke’s full force.

    “Our experiment shows a new relationship between the brain and the intestine,” said Dr. Josef Anrather, the Finbar and Marianne Kenny Research Scholar in Neurology and an associate professor of neuroscience in the Feil Family Brain and Mind Research Institute at Weill Cornell Medicine. “The intestinal microbiota shape stroke outcome, which will have an impact how the medical community views stroke and defines stroke risk.”

    The findings suggest that modifying the microbiotic makeup of the gut can become an innovative method to prevent stroke. This could be especially useful to high-risk patients, like those undergoing cardiac surgery or those who have multiple obstructed blood vessels in the brain.

    Further investigation is needed to understand exactly which bacterial components elicited their protective message. However, the researchers do know that the bacteria did not interact with the brain chemically, but rather influenced neural survival by modifying the behavior of immune cells. Immune cells from the gut made their way to the outer coverings of the brain, called the meninges, where they organized and directed a response to the stroke.

    “One of the most surprising findings was that the immune system made strokes smaller by orchestrating the response from outside the brain, like a conductor who doesn’t play an instrument himself but instructs the others, which ultimately creates music,” said Dr. Costantino Iadecola, director of the Feil Family Brain and Mind Research Institute and the Anne Parrish Titzell Professor of Neurology at Weill Cornell Medicine.

    The newfound connection between the gut and the brain holds promising implications for preventing stroke in the future, which the investigators say might be achieved by changing dietary habits in patients or “at risk” individuals.

    “Dietary intervention is much easier to accomplish than drug use, and it could reach a broad base,” Anrather said. “This is a little far off from the current study – it’s music of the future. But diet has the biggest effect of composition of microbiota, and once beneficial and deleterious species are identified, we can address them with dietary intervention.”

    See the full article here .

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    Once called “the first American university” by educational historian Frederick Rudolph, Cornell University represents a distinctive mix of eminent scholarship and democratic ideals. Adding practical subjects to the classics and admitting qualified students regardless of nationality, race, social circumstance, gender, or religion was quite a departure when Cornell was founded in 1865.

    Today’s Cornell reflects this heritage of egalitarian excellence. It is home to the nation’s first colleges devoted to hotel administration, industrial and labor relations, and veterinary medicine. Both a private university and the land-grant institution of New York State, Cornell University is the most educationally diverse member of the Ivy League.

    On the Ithaca campus alone nearly 20,000 students representing every state and 120 countries choose from among 4,000 courses in 11 undergraduate, graduate, and professional schools. Many undergraduates participate in a wide range of interdisciplinary programs, play meaningful roles in original research, and study in Cornell programs in Washington, New York City, and the world over.

     
  • richardmitnick 4:50 pm on March 28, 2016 Permalink | Reply
    Tags: , Medicine, ,   

    From phys.org: “New nanoparticle reveals cancer treatment effectiveness in real time” 

    physdotorg
    phys.org

    March 28, 2016

    1
    Using reporter nanoparticles loaded with either a chemotherapy or immunotherapy, researchers could distinguish between drug-sensitive and drug-resistant tumors in a pre-clinical model of prostate cancer. Credit: Ashish Kulkarni, Brigham and Women’s Hospital

    Being able to detect early on whether a cancer therapy is working for a patient can influence the course of treatment and improve outcomes and quality of life. However, conventional detection methods—such as PET scans, CT and MRI—usually cannot detect whether a tumor is shrinking until a patient has received multiple cycles of therapy.

    A new technique developed in pre-clinical models by investigators at Brigham and Women’s Hospital (BWH) offers a new approach and a read out on the effectiveness of chemotherapy in as few as eight hours after treatment. The technology can also be used for monitoring the effectiveness of immunotherapy. Using a nanoparticle that delivers a drug and then fluoresces green when cancer cells begin dying, researchers were able to visualize whether a tumor is resistant or susceptible to a particular treatment much sooner than currently available clinical methods.

    The team’s findings are published online this week in The Proceedings of the National Academy of Sciences.

    “Using this approach, the cells light up the moment a cancer drug starts working. We can determine if a cancer therapy is effective within hours of treatment,” said co-corresponding author Shiladitya Sengupta, PhD, a principal investigator in BWH’s Division of Bioengineering. “Our long-term goal is to find a way to monitor outcomes very early so that we don’t give a chemotherapy drug to patients who are not responding to it.”

    The new technique takes advantage of the fact that when cells die, a particular enzyme known as caspase is activated. The researchers designed a ‘reporter element’ that, when in the presence of activated caspase, glows green. The team then tested whether they could use the reporter nanoparticles to distinguish between drug-sensitive and drug-resistant tumors. Using nanoparticles loaded with anti-cancer drugs, the team tested a common chemotherapeutic agent, paclitaxel, in a pre-clinical model of prostate cancer and, separately, an immunotherapy that targets PD-L 1 in a pre-clinical model of melanoma. In the tumors that were sensitive to paclitaxel, the team saw an approximately 400 percent increase in fluorescence compared to tumors that were not sensitive to the drug. The team also saw a significant increase in the fluorescent signal in tumors treated with the anti-PD-L1 nanoparticles after five days.

    “We’ve demonstrated that this technique can help us directly visualize and measure the responsiveness of tumors to both types of drugs,” said co-corresponding author Ashish Kulkarni, an instructor in the Division of Biomedical Engineering at BWH. “Current techniques, which rely on measurements of the size or metabolic state of the tumor, are sometimes unable to detect the effectiveness of an immunotherapeutic agent as the volume of the tumor may actually increase as immune cells begin to flood in to attack the tumor. Reporter nanoparticles, however, can give us an accurate read out of whether or not cancer cells are dying.”

    Researchers now plan to focus on the design of radiotracers that can be used in humans, and tests of both safety and efficacy will be necessary before the current technique can be translated into clinical applications. Sengupta, Kulkarni and their colleagues are actively working on these steps in order to further the lab’s goal of improving the management and treatment of cancer using nanotechnology.

    More information: Reporter nanoparticle that monitors its anticancer efficacy in real time, PNAS, http://www.pnas.org/cgi/doi/10.1073/pnas.1603455113

    See the full article here .

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    About Phys.org in 100 Words

    Phys.org™ (formerly Physorg.com) is a leading web-based science, research and technology news service which covers a full range of topics. These include physics, earth science, medicine, nanotechnology, electronics, space, biology, chemistry, computer sciences, engineering, mathematics and other sciences and technologies. Launched in 2004, Phys.org’s readership has grown steadily to include 1.75 million scientists, researchers, and engineers every month. Phys.org publishes approximately 100 quality articles every day, offering some of the most comprehensive coverage of sci-tech developments world-wide. Quancast 2009 includes Phys.org in its list of the Global Top 2,000 Websites. Phys.org community members enjoy access to many personalized features such as social networking, a personal home page set-up, RSS/XML feeds, article comments and ranking, the ability to save favorite articles, a daily newsletter, and other options.

     
  • richardmitnick 11:30 am on March 25, 2016 Permalink | Reply
    Tags: , Medicine, Paper Diagnostic Tests Could Save Thousands of Lives,   

    From SA: “Paper Diagnostic Tests Could Save Thousands of Lives” 

    Scientific American

    Scientific American

    March 25, 2016
    Prachi Patel

    1
    DFA Livertest: Postage stamp-sized paper tests developed by the non-profit Diagnostics for All can screen for drug toxicity by measuring enzymes produced by liver cells. Courtesy of Diagnostics for All, Inc.

    When someone with a high fever walks into a rural African clinic, diagnosis could be murky. The symptoms could be those of dengue, Ebola, West Nile disease, malaria or flu, and blood work results from distant labs, if available, often takes days. Now a handful of researchers are separately working on inexpensive, paper-based diagnostic tests that accurately pinpoint the cause of a disease in minutes and could speed up treatment and prevent its spread. The lack of funds and commercial partners however, means most might languish in labs.

    Experimental paper sensors that detect chemical or biological molecules have proved to be easy to use without the need for pricy equipment or trained specialists. They can cost pennies and they promise to be more sensitive than the rapid diagnostic kits on the market today. What’s more, they could have broader applications, such as treating neglected tropical diseases, mostly because pharmaceutical companies are focusing on widespread maladies that have a larger market. In addition to saving hundreds of thousands of lives each year in the developing world, these paper-based tests could stem health care costs by allowing home-based disease testing in developed regions.

    Despite their numerous benefits, however, there’s a risk that most of these devices might never fulfill their promise.

    Mini-laboratories

    Pharmaceutical companies already sell millions of rapid, paper-based tests priced between $1 and $2 for HIV, hepatitis C and tuberculosis, among other diseases. These are simple lateral-flow systems akin to home pregnancy tests: A strip of paper wicks urine or blood from one end to the other where chemicals or antibodies in the sample interact with an appropriate reagent, creating a color change. But their simplicity is also a limitation. “They work, but they are black or white and they test for one thing,” says Harvard University chemist George Whitesides.

    Whitesides and others have in the last decade pioneered new tests that are intricate mini-laboratories on paper. Like microfluidic chips, the paper devices can separate, mix, filter and concentrate fluids as well as perform timed reactions and control their sequence—all by patterning networks of fluid-wicking channels on paper. Whitesides does this patterning using wax on postage stamp–size pieces of filter paper patterned with wax to create tiny channels and compartments. His team uses inkjet printers to lay down these features, so they cost only a few pennies to make. He has also patented 3-D devices in which fluids flow along and between the layers for more complex processes.

    Unlike lateral-flow tests sold today “paper microfluidic devices can do more complex tests that require multiple processing steps,” says Ali Yetisen, a chemical engineer and biotechnologist at Harvard Medical School. For instance, they could repeat a test for accuracy or for multiple diseases at a time or measure precise levels of target molecules. And, they require no sample preparation.

    Paul Yager, a biochemist at the University of Washington, meanwhile, has developed a handheld plastic device the size of two stacked card decks that contains strips of patterned paper and wells containing reagents and dyes, and into which a user would insert a fluid sample. The patterns of dots that appear after 20 minutes could be read by a clinician or sent via smartphone camera to a physician elsewhere. Yager says that the box could cost as little as $1 to manufacture in bulk.

    Killer app

    With grants from the Defense Advanced Research Projects Agency (DARPA), both Yager and Whitesides are working on the killer app for paper microfluidics: nucleic acid testing. This would enable a medical practitioner to diagnosis a number of infectious and chronic diseases by detecting gene sequences or pathogen DNA. “The aim is to come up with a standard footprint for a paper-based nucleic acid test where you simply change one or two molecules to test for a different disease,” Yager says. Currently, nucleic acid detection is performed using the lab-based polymerase chain reaction (PCR) test, which makes copies of DNA strands. “If someone were to develop completely paper-based PCR, that would be revolutionary,” Yetisen says.

    But because PCR requires a series of temperature cycles, Yager and Whitesides use what’s called isothermal amplification, which is carried out at a constant temperature range of 60 to 65 degrees Celsius. The challenge is to find a cheap, disposable heating mechanism. Yager’s group has made a prototype device that can accurately spot the antibiotic-resistant MRSA bacteria and are working on Zika virus test. But the device uses batteries to power a heating circuit. The researchers are experimenting with using tea bag–size sachets filled with 100-micrometer-wide iron and magnesium pellets, similar to the what’s used in hand warmers, to create the necessary heat chemically. Meanwhile Whitesides and his colleagues have made a paper machine that can detect nucleic acids using a handheld UV source and camera phone. The test costs less than $2 but requires an incubator for heating. The team is developing a built-in electronic heater.

    A handful of companies are trying to test and deploy paper microfluidics in the developing world. Diagnostics for All, a nonprofit Whitesides started in 2007, is at the last stage of regulatory approval for a liver-toxicity test for patients who take potent liver-damaging drugs. The device measures the level of an enzyme released by liver cells when they break down. The firm is also developing a nucleic acid test for hepatitis C and HIV, says company CEO Marcus Lovell-Smith.

    Bellevue, Wash.–based Intellectual Ventures is testing two products: One is a $2 malaria test that is over 100 times more sensitive than today’s lateral-flow tests, says Bernhard Weigl, a flow-based diagnostics researcher at the company. Researchers there are also developing an easy urine test for tuberculosis. Today’s strips require coughing up phlegm, which is difficult for sick patients.

    Yet to date, most paper microfluidics remain proofs-of-concept. Part of the problem is taking a lab wonder to something that is robust and reliable in often hot, humid climates. “It’s very easy to make relatively cool devices but hard to make them reproducible,” Weigl says.

    The biggest challenge is a lack of funding for trials, regulatory approvals and manufacturing. “We’ve shown a path and done exciting early work,” Smith says. “But these are immensely expensive projects. It’s tens of millions of dollars to get these tests approved.”

    Yetisen points out the general lack of funding in the area of tropical diseases because the return for pharmaceutical companies is low. Whitesides is now in talks with two big non-U.S. industrial partners who are interested in paper microfluidic devices for uses other than tropical diseases. “The hope,” he says, “is that we can have a partner develop a platform for an application they’re interested in and then leverage the capital to develop what could be useful in Mumbai or Kinshasa.”

    See the full article here .

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    Scientific American, the oldest continuously published magazine in the U.S., has been bringing its readers unique insights about developments in science and technology for more than 160 years.

     
  • richardmitnick 9:15 am on March 25, 2016 Permalink | Reply
    Tags: , Clogged-up immune cells explain smoking risk for TB, Medicine,   

    From U Washington: “Clogged-up immune cells explain smoking risk for TB” 

    U Washington

    University of Washington

    03.24.2016
    Craig Brierley

    1
    Heavily clogged macrophage, a type of immune cell, that were stained with a dye that labels their lysosomes red.

    Smoking increases an individual’s risk of developing tuberculosis, or TB. Smoking also makes the infection worse, because it causes vital immune cells to become clogged up. This slows their movement and impedes their ability to fight infection, according to new research published in the journal Cell.

    Russell Berg and Steven Levitte, graduate students in the Medical Scientist Training Program at the University of Washington in Seattle were the lead authors of study. The senior author was Lalita Ramakrishnan, formerly of UW Medicine and now in the Department of Medicine at Cambridge University in the United Kingdom.

    TB is an infectious disease caused by Mycobacterium tuberculosis. The pathogen primarily infects the lungs, but can also infect other organs. It is transmitted from person to person through the air. The disease can cause breathlessness and wasting, and can lead to death. While treatments do exist, the drug regimen is one of the longest for any curable disease: a patient will typically need to take medication for six months.

    For people exposed to TB, the biggest risk factor for infection is exposure to smoke from active and passive cigarette smoking and from burning fuels. This risk is even greater than co-infection with HIV. However, until now it was unclear why smoke should increase this risk.

    When TB enters the body, the first line of defence it encounters are immune cells known as macrophages (Greek for ‘big eater’). This type of cell engulfs the bacterium and tries to break it down. In many cases, the macrophage is successfully prevents TB infection by killing the pathogen.

    In some cases, however, TB manages not just to avoid destruction, but also to use macrophages as ‘taxi cabs’ to drive deep into the host, thereby spreading the infection. TB’s next step is to cause infected macrophages to form tightly organized clusters known as tubercles, or granulomas.

    2
    Picture of a granuloma (without necrosis) as seen through a microscope on a glass slide. The tissue on the slide is stained with two standard dyes (hematoxylin: blue, eosin: pink) to make it visible. The granuloma in this picture was found in a lymph node of a patient with Mycobacterium avium infection. Sanjay Mukhopadhyay

    Once again, the macrophages and bacteria battle. If the macrophages lose, the bacteria use their advantage within this structure to spread from cell to cell.

    The international team of scientists reporting this week in Cell studied genetic variants that increase susceptibility to TB in zebrafish, a ‘see-through’ animal model for studying the disease. They identified a mutation linked to lysosomal deficiency disorders. The lysosome is an important component of macrophages responsible for destroying bacteria. This particular mutation caused a deficiency in an enzyme known as cathepsin, which acts like scissors within the lysosome to chop up bacteria. This mutation, however, would not necessarily explain why the macrophages could not destroy the bacteria, as other enzymes could take cathepsin’s place.

    The key, the researchers found, lay in a second property of the macrophage: housekeeping. As well as destroying bacteria, the macrophage also recycles unwanted material from within the body for reuse. Lysosomal deficiency disorders were preventing this essential operation.

    Ramakrishnan, the study’s senior author, explained: “Macrophages act a bit like vacuum cleaners within the body by vacuuming up debris and unwanted material, including the billions of cells that die each day as part of natural turnover. But the defective macrophages are unable to recycle this debris and get clogged up. They grow bigger, fatter and less able to move around and clear up other material.

    “This can become a problem in TB because once the TB granuloma forms, the host’s best bet is to send in more macrophages at a slow steady pace to help the already infected macrophages.”

    “When these distended macrophages can’t move into the TB granuloma,” added study co-author Levitte, “the infected macrophages that are already in there burst. This leaves a ‘soup’ in which the bacteria can grow, spread further and make the infection worse.”

    The researchers looked at whether the effect seen in the lysosomal deficiency disorders, where the clogged-up macrophage could no longer perform its work, would also be observed if the lysosome became clogged up with non-biological material. By ‘infecting’ the zebrafish with microscopic plastic beads, they were able to replicate this effect.

    “We saw that accumulation of material inside of macrophages by many different means, both genetic and acquired, led to the same result: macrophages that could not respond to infection,” explained co-author Russell Berg.

    This discovery then led the team to see whether the same phenomenon occurred in humans. Working with Joe Keane and his colleagues from Trinity College Dublin, Ireland, the researchers showed that the macrophages of smokers were similarly clogged up with smoke particles. This observation helped explain why people exposed to smoke were at a greater risk of TB infection.

    “Macrophages are our best shot at getting rid of TB. If they are slowed down by smoke particles, their ability to fight infection is going to be greatly reduced,” said Keane. “We know that exposure to cigarette smoke or smoke from burning wood and coal, for example, are major risk factors for developing TB. Our finding helps explain why this is the case. The good news is that stopping smoking reduces the risk by allowing the impaired macrophages to die away and be replaced by new, agile cells.”

    Also contributing to this research were David Tobin from Duke University, Cecilia Moens from the Fred Hutchinson Cancer Research Institute, C.J. Cambier and J. Cameron from University of Washington, Kevin Takaki from University of Cambridge, and Seonadh O’Leary and Mary O’Sullivan from Trinity College Dublin.

    Their findings were reported in the March 24 Cell article, Lysosomal Disorders Drive Susceptibility to Tuberculosis by Compromising Macrophage Migration (10.1016/j.cell.2016.02.034)

    The research was supported by the National Institutes of Health, the University of Washington Medical Scientist Training Program, the Wellcome Trust, the National Institute of Health Research Cambridge Biomedical Research Centre, the Health Research Board of Ireland and The Royal City of Dublin Hospital Trust.

    Media Contacts:

    Cambridge University, U.K.: Craig Brierley, +44 (0)1223 766205, Craig.Brierley@admin.cam.ac.uk
    University of Washington, Seattle: Leila Gray, 206-685-0381, leilag@uw.edu

    See the full article here .

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    The University of Washington is one of the world’s preeminent public universities. Our impact on individuals, on our region, and on the world is profound — whether we are launching young people into a boundless future or confronting the grand challenges of our time through undaunted research and scholarship. Ranked number 10 in the world in Shanghai Jiao Tong University rankings and educating more than 54,000 students annually, our students and faculty work together to turn ideas into impact and in the process transform lives and our world. For more about our impact on the world, every day.

    So what defines us — the students, faculty and community members at the University of Washington? Above all, it’s our belief in possibility and our unshakable optimism. It’s a connection to others, both near and far. It’s a hunger that pushes us to tackle challenges and pursue progress. It’s the conviction that together we can create a world of good. Join us on the journey.

     
  • richardmitnick 7:36 am on March 25, 2016 Permalink | Reply
    Tags: , Help Stop TB project, Medicine,   

    Help Stop TB from WCG: “Researchers Partner with World Community Grid to Help Stop a Leading Killer” 

    New WCG Logo
    WCGLarge

    WCG Help Stop TB
    WCG Help Stop TB. No image credit

    24 Mar 2016
    By: Dr. Anna Croft
    University of Nottingham, UK

    Summary
    Tuberculosis is one of the world’s most prevalent and deadly infectious diseases. Researchers from the University of Nottingham, UK, have partnered with World Community Grid to take a close look at the bacterium that causes tuberculosis, so that scientists can develop more effective treatments.


    Access mp4 video here .

    Tuberculosis (TB) is one of the biggest global killers. In 2014, there were 9.6 million newly diagnosed cases and more than 1.5 million people who died from the disease. More than 1 million of these new cases, and 140,000 deaths, were estimated for children. The World Health Organization has declared TB to be the world’s deadliest infectious disease, along with HIV. To help combat this disease, my team and I are working with World Community Grid on a new project called Help Stop TB.

    TB is caused by infection from a bacterium known as Mycobacterium tuberculosis (M. tb). Typical symptoms of an active TB infection include persistent cough, fever, loss of weight, and night sweats. If the infection is left untreated, the bacteria are likely to cause increased damage to the lungs and spread throughout the body, which may ultimately lead to death. Treatment for an uncomplicated TB infection lasts more than six months and requires a combination of antibiotics.

    I am an associate professor in the Department of Chemical and Environmental Engineering at the University of Nottingham, UK. My team and I seek to improve the understanding, and therefore the treatment, of TB. To do this, we are excited to partner with World Community Grid and its community of volunteers to study and understand the protective outer coating of M. tb, and learn how to penetrate its defenses.

    The Research Team

    TB knows no boundaries. Luckily, neither does the research team that seeks to shed light on the molecular mysteries of this disease. We have come to the University of Nottingham from various parts of the world to conduct research into a disease that has a large global impact.

    As a young girl in Australia, I was very interested in the chemical underpinnings of medicine and human biology. My mother was keen for me to become a physician, but I had my heart set on a career in science. I remember saying, “I will be a doctor, but not that kind of doctor.” I chose to study Chemistry and Biochemistry, and became a researcher in order to have an impact on the health of a great number of people.

    A few years ago, I was conducting research on mycolic acids, which are long fatty acids in the cell walls of certain bacteria, including M. tb. Through this research, I met Wilma Groenewald, who began studying TB while she was an undergraduate at the University of Pretoria in South Africa. There is a large population of TB patients in South Africa, including people with complex diagnoses, and Wilma began studying the disease to make a difference in the health of her home country.

    The Help Stop TB research team also includes Athina Meletiou, who is from Greece, and Christof Jäger, hailing from Germany, who provide expertise in computational modeling and molecular dynamics. Additionally, we are lucky to work with David Burgess, who is originally from Berkshire and will oversee the IT needs of the project. We all share a determination to build on the work of previous researchers as we take on a disease that has proved to be highly resistant to most drugs.

    1
    Members of the Help Stop TB research team: Christof Jäger, Wilma Groenewald, Athina Meletiou and Anna Croft

    Scientists have learned that M. tb, which causes TB, has a highly unusual cell wall made up of mycolic acids, which protects it from incoming drugs and from a person’s own immune system. Bacterial resistance against the drugs available to treat TB is on the increase throughout the world, and is making TB treatment more challenging. This resistance typically develops when patients don’t complete their long courses of treatment, which can take from six months to two years, giving the bacteria an opportunity to evolve resistance to the drugs that were used.

    Additionally, TB infection is a particular challenge in areas where HIV infection is high, because HIV patients can be susceptible to contracting TB due to their suppressed immune systems. The World Health Organization reports that in 2015, one in three HIV deaths was due to TB.

    Our Goals

    By enlisting the help of World Community Grid volunteers, we plan to simulate different variations of the mycolic acid structures within the cell wall of M. tb to understand how these variations impact the functioning of the bacterium. This will help us develop a more complete and cohesive model of the cell wall, and better understand the role these mycolic acids play in protecting the TB bacterium. This basic research will in turn help scientists develop treatments to attack the disease’s natural defenses.

    We would not be able to undertake the necessary big data approach to understand the structure of these mycolic acids without World Community Grid’s computational power. With access to this power, we can observe many different mycolic acid structure models instead of just a few. We hope you will donate your unused computing power to the fight against one of the world’s most widespread and deadly infectious diseases.

    To contribute to Help Stop TB, join World Community Grid [link is below], or if you are already a volunteer, make sure the project is selected on your My Projects page.

    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.

    BOINC WallPaper

    CAN ONE PERSON MAKE A DIFFERENCE? YOU BETCHA!!

    “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.

    Please visit the project pages-

    Help Stop TB
    WCG Help Stop TB

    Outsmart Ebola together

    Outsmart Ebola Together

    Mapping Cancer Markers
    mappingcancermarkers2

    Uncovering Genome Mysteries
    Uncovering Genome Mysteries

    Say No to Schistosoma

    GO Fight Against Malaria

    Drug Search for Leishmaniasis

    Computing for Clean Water

    The Clean Energy Project

    Discovering Dengue Drugs – Together

    Help Cure Muscular Dystrophy

    Help Fight Childhood Cancer

    Help Conquer Cancer

    Human Proteome Folding

    FightAIDS@Home

    World Community Grid is a social initiative of IBM Corporation
    IBM Corporation
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    IBM – Smarter Planet
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