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  • richardmitnick 10:35 am on May 25, 2016 Permalink | Reply
    Tags: , , , Medicine, Nerve damage found in prediabetics   

    From Hopkins via The Baltimore Sun: “Nerve damage found in prediabetics” Why to Avoid Dunkin’ Donuts 

    Johns Hopkins
    Johns Hopkins University

    1

    5.25.16
    Andrea K. McDaniels

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    Michael Jackson suffers from significant nerve damage stemming from prediabetes. (Lloyd Fox / Baltimore Sun)

    The pain shot across the tops of Michael Jackson’s feet as if someone was pounding him with a sledgehammer, sometimes becoming so unbearable he couldn’t sleep.

    The aerospace engineer blamed it on arthritis until his primary care physician ruled that out. Tests for Lupus and Lou Gherig’s disease also came back negative. Finally, a doctor cut a small sample of skin from one of Jackson’s feet and counted the nerve fibers under a microscope.

    Jackson suffered from significant nerve damage stemming from prediabetes — a condition in which people have high blood glucose levels but not enough to be classified as diabetes.

    Doctors have known for a while that those with prediabetes can experience mild weakness, numbness and pain from nerve damage, but a new Johns Hopkins study suggests that so-called neuropathy is much more significant than once thought. Like Jackson, patients can experience excruciating pain more typically associated with full-blown diabetes. About 50 percent of people with diabetes have neuropathy, according to the National Institute of Neurological Disorders and Stroke.

    The numbness associated with neuropathy can contribute to some diabetics’ eventual need for amputation. Diabetics tend to have poor blood circulation, which can lead to infection and ulcers. A patient may not notice an injury or infection due to lack of feeling, leading to amputation.

    The Johns Hopkins researchers say their findings provide evidence that patients should be screened for prediabetes and neuropathy much earlier than once thought. The medical community also needs to do a better job at treating and diagnosing those with prediabetes, the researchers concluded. An estimated one in three Americans — 86 million people — have prediabetes, according to the U.S. Centers for Disease Control, and may be at particular risk to the unknown consequences of the disease.

    “It means that even mild blood sugar elevations are important and it’s important for us to be aggressive in how we treat that,” said Dr. Michael Polydefkis, the study’s senior author and a professor of neurology at the Johns Hopkins University School of Medicine and director of the Cutaneous Nerve Lab.

    The Hopkins study is different from those done in the past because it showed deterioration over the entire length of sensory nerve fibers and not just at the ends, which suggests the damage is not localized.

    The patients with prediabetes, studied over a period of three years, continued to have worsening damage to their small nerve fibers throughout the study just as patients with full-blown diabetes did. Skin samples taken from the ankle, thigh and knee showed a 10 percent loss in the density of nerve cells by the end of the study.

    “I expected that people with diabetes would do worse, but I didn’t really expect people with prediabetes to experience a similar rate of degradation of their small nerve fibers,” Polydefkis said.

    The results come as medical providers already are trying to better diagnose prediabetes.

    For the last few years, the American Medical Association has worked to increase public awareness about prediabetes and get more phyisicians to screen at-risk patients. Working with the U.S. Centers for Disease Control, the association is offering doctors more information about prevention programs for their patients.

    The medical association also is participating in a public service campaign to raise awareness of prediabetes as a serious health problem. The campaign encourages people to find out if they have prediabetes and to take steps to reverse their condition to avoid developing full diabetes.

    If caught early, prediabetes can be treated with lifestyle changes, such as weight loss, exercise and diet modification to bring blood sugar levels down. Some doctors also believe the medicine used to treat diabetes could be used for prediabetes as well.

    Untreated prediabetes could progress to diabetes and lead to lifelong health problems, including cardiovascular disease and skin problems. Diabetes can destroy the blood vessels of the retina leading to blindness and damage the kidneys, which the body uses to filter out waste, leading some patients to need dialysis treatment to survive. Research shows that 15 percent to 30 percent of overweight people with prediabetes will develop type 2 diabetes within five years unless they make lifestyle changes.

    “We know that people who take preventive measures early on can slow the rate of decline,” said Dr. Ruth S. Horowitz, chief of the division of endocrinology and metabolism at Greater Baltimore Medical Center.

    There are some limits to the study. The sample size was small with 62 people, including 16 who were prediabetic and 52 with tingling and pain in their hands and feet.

    Still, the Hopkins research could help convince insurance companies to eventually cover the treatment of prediabetes, some doctors said. Insurance companies don’t always cover nutritional education and supplies for glucose testing until a patient has full-blown diabetes.

    “This study reinforces the need for us to address prediabetes as an even more serious problem,” said Stephen N. Davis, chair of the department of medicine at the University of Maryland School of Medicine. “It really does show there are consequences with prediabetes.”

    Jackson continues to cope with the consequences of his neuropathy. His nerve damage has gotten worse over time. He has lost much of the feeling in his feet and once dropped a cinder block on his foot without knowing until he looked down. His balance is off and he sometimes finds himself falling over in the shower. He is trying to manage the condition with medications and eating better.

    “As a kid I ate a lot of candy,” he said. “I was drowning myself with sugar as a kid, but back in the day nobody said much about sugar. I have tried to cut back now and it has helped.”

    See the full article here .

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    Johns Hopkins Campus

    The Johns Hopkins University opened in 1876, with the inauguration of its first president, Daniel Coit Gilman. “What are we aiming at?” Gilman asked in his installation address. “The encouragement of research … and the advancement of individual scholars, who by their excellence will advance the sciences they pursue, and the society where they dwell.”

    The mission laid out by Gilman remains the university’s mission today, summed up in a simple but powerful restatement of Gilman’s own words: “Knowledge for the world.”

    What Gilman created was a research university, dedicated to advancing both students’ knowledge and the state of human knowledge through research and scholarship. Gilman believed that teaching and research are interdependent, that success in one depends on success in the other. A modern university, he believed, must do both well. The realization of Gilman’s philosophy at Johns Hopkins, and at other institutions that later attracted Johns Hopkins-trained scholars, revolutionized higher education in America, leading to the research university system as it exists today.

     
  • richardmitnick 9:00 pm on May 24, 2016 Permalink | Reply
    Tags: 'Kidney on a chip', , Medicine,   

    From U Michigan: ” ‘Kidney on a chip’ could lead to safer drug dosing” 

    U Michigan bloc

    University of Michigan

    5/4/2016
    Gabe Cherry, Michigan Engineering

    1
    No image caption, no image credit

    University of Michigan researchers have used a “kidney on a chip” device to mimic the flow of medication through human kidneys and measure its effect on kidney cells. The new technique could lead to more precise dosing of drugs, including some potentially toxic medicines often delivered in intensive care units.

    Precise dosing in intensive care units is critical, as up to two-thirds of patients in the ICU experience serious kidney injury. Medications contribute to this injury in more than 20 percent of cases, largely because many intensive care drugs are potentially dangerous to the kidneys.

    Determining a safe dosage, however, can be surprisingly difficult. Today, doctors and drug developers rely mainly on animal testing to measure the toxicity of drugs and determine safe doses. But animals process medications more quickly than humans, making it difficult to interpret test results and sometimes leading researchers to underestimate toxicity.

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    No image caption, no image credit

    The new technique offers a more accurate way to test medications, closely replicating the environment inside a human kidney. It uses a microfluidic chip device to deliver a precise flow of medication across cultured kidney cells. This is believed to be the first time such a device has been used to study how a medication behaves in the body over time, called its “pharmacokinetic profile.”

    “When you administer a drug, its concentration goes up quickly and it’s gradually filtered out as it flows through the kidneys,” said University of Michigan Biomedical Engineering professor Shuichi Takayama, an author on the paper. “A kidney on a chip enables us to simulate that filtering process, providing a much more accurate way to study how medications behave in the body.”

    Takayama said the use of an artificial device provides the opportunity to run test after test in a controlled environment. It also enables researchers to alter the flow through the device to simulate varying levels of kidney function.

    “Even the same dose of the same drug can have very different effects on the kidneys and other organs, depending on how it’s administered,” said Sejoong Kim, an associate professor at Korea’s Seoul national University Budang Hospital, former U-M researcher and author on the paper. “This device provides a uniform, inexpensive way to capture data that more accurately reflects actual human patients.”

    In the study, the team tested their approach by comparing two different dosing regimens for gentamicin, an antibiotic that’s commonly used in intensive care units. They used a microfluidic device that sandwiches a thin, permeable polyester membrane and a layer of cultured kidney cells between top and bottom compartments.

    3
    No image caption, no image credit

    They then pumped a gentamicin solution into the top compartment, where it gradually filtered through the cells and the membrane, simulating the flow of medication through a human kidney. One test started with a high concentration that quickly tapered off, mimicking a once-daily drug dose. The other test simulated a slow infusion of the drug, using a lower concentration that stayed constant. Takayama’s team then measured damage to the kidney cells inside the device.

    They found that a once-daily dose of the medication is significantly less harmful than a continuous infusion—even though both cases ultimately delivered the same dose of medication. The results of the test could help doctors better optimize dosing regimens for gentamicin in the future. Perhaps most importantly, they showed that a kidney on a chip device can be used to study the flow of medication through human organs.

    “We were able to get results that better relate to human physiology, at least in terms of dosing effects, than what’s currently possible to obtain from common animal tests,” Takayama said. “The goal for the future is to improve these devices to the point where we’re able to see exactly how a medication affects the body from moment to moment, in real time.”

    Takayama said the techniques used in the study should be generalizable to a wide variety of other organs and medications, enabling researchers to gather detailed information on how medications affect the heart, liver and other organs. In addition to helping researchers fine-tune drug dosing regimens, he believes the technique could also help drug makers test drugs more efficiently, bringing new medications to market faster.

    Within a few years, Takayama envisions the creation of integrated devices that can quickly test multiple medication regimens and deliver a wide variety of information on how they affect human organs. PHASIQ, an Ann Arbor-based spinoff company founded by Takayama is commercializing the biomarker readout aspect of this type of technology in conjunction with the University of Michigan Office of Technology Transfer, where Takayama serves as a Faculty Innovation Ambassador.


    Access mp4 video here .
    University of Michigan researchers used a “kidney on a chip” to mimic the flow of medication through human kidneys. This enabled them to study the dosing regimen for a common intensive care drug. No video credit

    The paper, published in the journal Biofabrication, is titled Pharmacokinetic profile that reduces nephrotoxicity of gentamicin in a perfused kidney-on-a-chip. Funding and assistance for the project was provided by the National Institutes of Health (grant number GM096040), the University of Michigan Center for Integrative Research in Critical Care (MCIRCC), the University of Michigan Biointerfaces Institute, the National Research Foundation of Korea and the Korean Association of Internal Medicine Research Grant 2015.

    See the full article here .

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    U MIchigan Campus

    The University of Michigan (U-M, UM, UMich, or U of M), frequently referred to simply as Michigan, is a public research university located in Ann Arbor, Michigan, United States. Originally, founded in 1817 in Detroit as the Catholepistemiad, or University of Michigania, 20 years before the Michigan Territory officially became a state, the University of Michigan is the state’s oldest university. The university moved to Ann Arbor in 1837 onto 40 acres (16 ha) of what is now known as Central Campus. Since its establishment in Ann Arbor, the university campus has expanded to include more than 584 major buildings with a combined area of more than 34 million gross square feet (781 acres or 3.16 km²), and has two satellite campuses located in Flint and Dearborn. The University was one of the founding members of the Association of American Universities.

    Considered one of the foremost research universities in the United States,[7] the university has very high research activity and its comprehensive graduate program offers doctoral degrees in the humanities, social sciences, and STEM fields (Science, Technology, Engineering and Mathematics) as well as professional degrees in business, medicine, law, pharmacy, nursing, social work and dentistry. Michigan’s body of living alumni (as of 2012) comprises more than 500,000. Besides academic life, Michigan’s athletic teams compete in Division I of the NCAA and are collectively known as the Wolverines. They are members of the Big Ten Conference.

     
  • richardmitnick 12:14 pm on May 23, 2016 Permalink | Reply
    Tags: , Medicine, , UW Medical Center ready to deploy tiniest pacemaker ever   

    From U Washington: “UW Medical Center ready to deploy tiniest pacemaker ever” 

    U Washington

    University of Washington

    05.20.2016
    Brian Donohue

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    The old and the new: a conventional pacemaker, left, and the Medtronic Micra are displayed by UW Medicine electrophysiologists Jordan Prutkin and Kristen Patton.

    The world’s smallest pacemaker will debut soon at UW Medical Center – one of two Washington state hospitals that will offer the device for the next several months.

    Drs. Jordan Prutkin and Kristen Patton, cardiac electrophysiologists with the UW Medicine Regional Heart Center, received final training this week from representatives of Medtronic, the manufacturer of the device, named Micra.

    About as tall and wide as a AAA battery, the device is threaded up through the femoral vein to the heart, where it is attached to the right ventricle to deliver impuses when a patient’s heartbeat is too slow. The unit’s direct placement takes advantage of another advance: Its battery is inside, so there are no wires connected to a separate power source.

    For decades, pacemakers have comprised a generator, usually implanted under the skin in the patient’s left chest, and leads, which carry impulses from the generator into the heart. The wires are these devices’ main vulnerability, wearing out over time and heightening risk of infections. Removing broken leads years after implant can be problematic because they often have become enmeshed within the tissue of blood vessels.

    “That’s why this miniature technology is so important and transformative – because it really does reduce risks associated with these devices,” Patton said.

    On April 6, the U.S. Food and Drug Administration approved the Micra for patients with slow or irregular heart rhythms. The FDA based its decision on a clinical trial of 719 patients implanted with the device. In the study, 98 percent of patients experienced adequate heart pacing and fewer than 7 percent had complications such as blood clots, heart injury and device dislocation.

    The risk of dislodgement is low, Patton said. “Its tiny hooks deploy straight into the muscle and grab and it is very hard to detach.”

    The Micra will have limited applicability, at least initially, because it paces only one chamber. About 75 percent of conventional pacemakers pace at least two of the heart’s chambers.

    “This is good for people who only need pacing in the ventricle because they have atrial fibrillation in the top chamber, and for people who only need pacing a small percentage of the time,” Prutkin said.

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    Illustration of the Micra being deployed into a right ventricle. Medtronic

    Similar to other single-chamber devices on the market, the Micra’s battery is projected to last 10 to 14 years, depending on how much pacing a patient requires.

    At the Micra training, Patton said, she heard something that she hadn’t expected.

    “The two physicians leading the session have a lot of experience with this device, and they said it makes a difference psychologically to patients; it removes the visible bump under the skin of the generator and that persistent reminder that ‘something is wrong with my heart.’

    “We hear from patients all the time, wondering whether they should move less to protect against lead fracture. Patients ask, ‘What if I wear a backpack? Can I still do pushups or play golf?’ This device seems to be a positive step in that way,” Patton said.

    Prutkin sees this device as the beginning of the next generation of pacemakers.

    “Right now this can only go in the ventricle, but in time this will be available for both the atria and ventricles, and multiple devices in one person will be able to talk to one another to regulate a heartbeat. That’s down the road, but that’s where this technology is heading.”

    The device also will be available at Sacred Heart Medical Center in Spokane.

    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 4:13 pm on May 21, 2016 Permalink | Reply
    Tags: , Heart disease and stroke risk predicted by new tools, , Medicine   

    From ICL: “Heart disease and stroke risk predicted by new tools” 

    Imperial College London
    Imperial College London

    21 May 2016
    Kate Wighton

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    Damage to blood vessels in eyes, kidneys and nerve cells may cause two-fold increased risk of heart attack or stroke in people with type 2 diabetes.

    Individuals with diabetes are susceptible to damage to small blood vessels in the eyes, kidneys and nerve cells that can, in turn, lead to blindness, kidney failure and leg amputation. In 2004, routine screening for this damage, known as microvascular disease, was introduced in the UK.

    The team, which included scientists from Imperial College London, St George’s, University of London, and St George’s University Hospitals NHS Foundation Trust, looked at data for 49,027 individuals with type 2 diabetes in the UK. They used this data to assess whether screening information on microvascular disease could also predict damage to the large blood vessels that causes heart attacks and stroke (cardiovascular disease).

    The researchers found any single sign of microvascular disease resulted in around a 30% increased risk of cardiovascular disease. Risk increased with each additional factor present such that the risk was increased two fold when all three were present. Researchers found that damage to small blood vessels in the eyes, kidneys and nerve cells were at least as strong an indication of the likelihood of later cardiovascular disease as many conventionally accepted risk factors – such as high blood pressure and cholesterol.

    Professor Kausik Ray, co-senior author from School of Public Health at Imperial said: “We found the presence of damage to the eyes, kidneys and nerves in combination incrementally doubled risk of cardiovascular disease, mortality and hospitalisation for heart failure. Our findings suggest that incorporating commonly available screening tests – that are already routinely assessed in those with diabetes – can significantly improve risk prediction. If applied globally, these findings have the potentially to improve therapeutic decision making in several millions of patients, simply by looking in the back of the eye, testing the feet with a microfilament and taking a dip stick test of the urine. It’s easy and cheap.”

    The data, published* in the journal Lancet Diabetes, suggests that continuing the screening programme for microvascular disease in GP practices is needed. Not only does this predict the risk of blindness, kidney failure and leg amputations, but it also provides a clear indication of whether an individual is likely to go on to develop cardiovascular disease.

    In the UK, NICE guidelines recommend that any individual who is 10% or more likely to experience cardiovascular disease in the next 10-years should be offered a statin prescription with the aim of preventing future heart attacks and strokes. When data on microvascular disease is included in the assessment of an individual patient’s risk of cardiovascular disease, an extra 135,000 people in the UK could be offered a statin prescription appropriately as their risk would cross this predicted threshold. Furthermore, 200,000 individuals would fall below the threshold for statin treatment and consequently these lower risk groups would not be offered a statin.

    The team argues this may mean earlier treatment for patients at higher risk of developing cardiovascular disease – in particular younger patients and women, who often are believed to be at low risk on the basis of age and gender. There are also potential cost benefits to the health service, by preventing more cardiovascular disease in higher risk patients. In addition to this, there would be fewer statin prescriptions – and so potentially fewer side effects – in low risk individuals.

    Co-Lead author, Jack Brownrigg, of St George’s University, added: “The study has identified a very high risk group of patients with diabetes. The number of people with diabetes in the UK is rising, driven largely by obesity. These results will help us to focus preventive treatments on those patients who are at most risk of developing cardiovascular disease and should reduce the number of people with diabetes who experience a heart disease or stroke”.

    *Science paper:
    Microvascular disease and risk of cardiovascular events among individuals with type 2 diabetes: a population-level cohort study

    See the full article here .

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    Imperial College London

    Imperial College London is a science-based university with an international reputation for excellence in teaching and research. Consistently rated amongst the world’s best universities, Imperial is committed to developing the next generation of researchers, scientists and academics through collaboration across disciplines. Located in the heart of London, Imperial is a multidisciplinary space for education, research, translation and commercialisation, harnessing science and innovation to tackle global challenges.

     
  • richardmitnick 5:23 pm on May 19, 2016 Permalink | Reply
    Tags: , Medicine, OpenZika project at World Community Grid, ,   

    From World Community Grid and Rutgers University: “Fighting the Zika Virus with the Power of Supercomputing” 

    Rutgers University

    New WCG Logo

    WCGLarge

    From Rutgers

    Thursday, May 19, 2016

    Rutgers Open Zika

    Rutgers is taking a leading role in an IBM-sponsored World Community Grid project that will use supercomputing power to identify potential drug candidates to cure the Zika virus.

    The project, known as OpenZika, employs a global team of scientists who will perform “virtual” experiments in a search of treatments for the fast-spreading virus that the World Health Organization has declared a global public health emergency.

    OpenZika will screen current drugs and millions of drug-like compounds from existing databases against models of Zika protein structures (and also against structures of proteins from related viruses, including West Nile Virus and Dengue). These computational results will be shared quickly with the research community and general public, with compounds showing the most promise then tested in laboratory settings.

    “Instead of having to wait a number of years, even decades potentially, to test all these compounds in order to find a few that could form the basis of antiviral drugs to cure Zika, we will perform these initial tests in a matter of months, just by using idle computing power that would otherwise go to waste,” says Alex Perryman, a research teaching specialist at Rutgers’ New Jersey Medical School, in Professor Joel Freundlich’s lab.

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    OpenZika co-principal investigator Alex Perryman, researcher at Rutgers’ New Jersey Medical School, also managed the World Community Grid’s first biomedical computing project, FightAIDS@Home, and its Global Online Fight Against Malaria (GO FAM). Perryman was selected as co-principal investigator of the OpenZika project, while Freundlich serves as a key consultant.

    Perryman was selected as co-principal investigator of the OpenZika project, while Freundlich serves as a key consultant.

    Rutgers’ Perryman has had deep experience working with IBM’s World Community Grid. From 2007 to 2013, he managed and performed the day-to-day duties required for FightAIDS@Home, the first biomedical computing project on World Community Grid. In 2011, Perryman designed, developed and ran the grid’s Global Online Fight Against Malaria (GO FAM) project, which has resulted in identifying promising tool compounds for treating malaria and drug-resistant tuberculosis.

    In less than two years, GO FAM volunteers on the grid performed more than a billion docking jobs, which, Perryman estimates, would have taken at least 100 years using the computer capacity found at most universities. The Freundlich lab has leveraged GO FAM data against tuberculosis drug targets, along with novel machine learning techniques they have developed, to seed novel therapeutic strategies.

    For the OpenZika project IBM is working with an international team of researchers, led by Federal University of Goias in Brazil; with scientists from the Oswaldo Cruz Foundation (Fiocruz) in Brazil; Rutgers University’s New Jersey Medical School (NJMS); and the University of California, San Diego (UCSD). Carolina Horta Andrade, professor at Federal University of Goias, is the principal investigator. Joining Perryman as co-PI is Sean Ekins, CEO, Collaborations Pharmaceuticals.

    Volunteers can support the OpenZika search for a cure by joining World Community Grid. IBM also invites researchers to submit research project proposals to receive this free resource. For more information about IBM’s philanthropic efforts, visit http://www.citizenIBM.com or follow @CitizenIBM on Twitter.

    From World Community Grid

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    Help an International Research Team Fight the Zika Virus

    19 May 2016
    By: Dr. Carolina Horta Andrade
    Universidade Federal de Goiás, Brazil

    Summary
    The Zika virus was relatively unknown until 2015, when it made headlines due its rapid spread and its link to severe brain-related deficiencies in newborns born to mothers who contracted the virus while pregnant. Dr. Carolina Horta Andrade, the principal investigator for the new OpenZika project, discusses how she and an international team of researchers are using World Community Grid to accelerate the search for an effective anti-Zika treatment.

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    Dr. Carolina Horta Andrade, principal investigator for OpenZika

    Introduction

    Few people had heard of the Zika virus before 2015, when it began rapidly spreading in the Americas, particularly in Brazil. The virus is mostly spread by Aedes aegypti mosquitoes, although sexual and blood transmission are also possible. A currently unknown percentage of pregnant women who have contracted the Zika virus have given birth to infants with a condition called microcephaly, which results in severe brain development issues. In other cases, adults and children who contract the Zika virus have suffered paralysis and other neurological problems.

    Currently, there is no treatment for the Zika virus and no vaccine. Given that Zika has quickly become an international public health concern, my team and I are working with researchers here in Brazil as well as in the United States to look for possible treatments, and we are using World Community Grid to accelerate our project.

    Background

    The world has become increasingly alarmed about the Zika virus, and with good reason. Until recently there has been little research on this disease, but in the past few months it has been linked to severe brain deficiencies in some infants as well as potential neurological issues in children and adults. As a scientist and a citizen of Brazil, which has been greatly affected by Zika, I am committed to the fight against the virus, but my team and I will need the help of World Community Grid volunteers to provide the massive computational power required for our search for a Zika treatment.

    I am a professor at the Universidade Federal de Goiás (UFG) in Brazil, and the director of LabMol, a university laboratory which searches for treatments for neglected diseases and cancer. My field is medicinal and computational chemistry, with an emphasis on drug design and discovery for neglected diseases. I first became interested in working in this area because these are diseases that do not interest pharmaceutical companies, since they mainly affect marginalized populations in underdeveloped and developing countries. However, these diseases are highly debilitating and, for most of them, there is no adequate drug treatment. Brazil is vulnerable to a number of neglected diseases, such as dengue, malaria, leishmaniasis, schistosomiasis, and others. My greatest desire is to find treatments to improve the lives of thousands of people throughout the world who suffer from these diseases.

    In 2015, I started a project in collaboration with Dr. Sean Ekins, a pharmacologist with extensive research experience, to focus on the development of computational models to identify active compounds against the dengue virus, which is a serious mosquito-borne disease found throughout the world. These active compounds could become candidates for antiviral drugs. We are now at the stage of selecting compounds to start laboratory tests. In January of 2016, when the Zika virus outbreak in Brazil became alarming, Sean and I decided to expand our dengue research, and we included the Zika virus in our work, since these two diseases are from the same family of viruses.

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    Dr. Sean Ekins, CEO, Collaborations Pharmaceuticals, Inc.

    Sean invited me and other collaborators to write a perspective paper that was published*in the beginning of 2016, about the need for open drug discovery for the Zika virus. This work grabbed the attention of scientific illustrator John Liebler, who wanted to produce a picture of the complete Zika virion. We are using the illustration he created (shown below) as a visual for the OpenZika project.

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    Image copyright John Liebler, http://www.ArtoftheCell.com. All rights reserved. Used by permission.

    John’s interest inspired us to try to model every protein in the Zika virus, which directly led to writing a groundbreaking paper** with homology models of all the proteins of the Zika virus. (Homology models, which are computational, three-dimensional renderings of proteins within an organism, are useful when the structure of a protein is not experimentally known, which is the case with the Zika virus.)

    The OpenZika Research Team

    After Sean and I began our work on the Zika virus, he introduced me to World Community Grid. Sean has also collaborated with Dr. Alexander Perryman of Rutgers University, New Jersey Medical School, who was previously at The Scripps Research Institute where he played a key role in two World Community Grid projects: Fight AIDS@Home and GO Fight Against Malaria. Sean and Alex are both co-principal investigators with me on the OpenZika project.

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    Dr. Alexander Perryman, co-primary investigator, and Dr. Joel Freundlich, collaborator, Rutgers University New Jersey Medical School

    The research team also includes my colleagues at UFG, Dr. Rodolpho Braga, Dr. Melina Mottin and Dr. Roosevelt Silva; Dr. Jair L. Siqueira-Neto from University of California, San Diego; and Dr. Wim Degrave of the Oswaldo Cruz Foundation in Brazil, who is already working with World Community Grid on the Uncovering Genome Mysteries project, among others.

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    The UFG team includes Dr. Rodolpho Braga, Dr. Carolina Horta Andrade, Dr. Melina Mottin and Dr. Roosevelt Silva (not pictured).

    This large group of collaborators means that the team has every set of skills and experience necessary to conduct this research end-to-end, as some of the researchers are computational modeling experts while others have extensive laboratory experience.

    Our Goals

    The OpenZika project on World Community Grid aims to identify drug candidates to treat the Zika virus in people who have been infected. The project will use software to screen millions of chemical compounds against the target proteins that the Zika virus likely uses to survive and spread in the human body, based on what is known from similar diseases such as dengue virus and yellow fever. As science’s knowledge of the Zika virus increases in the coming months and key proteins are identified, the OpenZika team will use the new knowledge to refine our search.

    Our work on World Community Grid is only the first step in the larger project of discovering a new drug to fight the Zika virus. Next, we will analyze the data obtained from World Community Grid’s virtual screening to choose the compounds that show the most promise. After we have selected and tested compounds that could be effective in killing the Zika virus, we will publish our results. As soon as we have proven that some of the candidate compounds can actually kill or disable the virus in cell-based tests, we and other labs can then modify the molecules to increase their potency against the virus, while ensuring that these modified compounds are safe and non-toxic.

    We are committed to releasing all the results to the public as soon as they are completed, so other scientists can help advance the development of some of these active compounds into new drugs. We hope that OpenZika will include a second stage, where we can perform virtual screenings on many more compounds.

    Without this research–and other projects that are studying the Zika virus–this disease could become an even bigger threat due to the rapid spread of the virus by mosquitoes, blood and sexual transmission. The link between the Zika virus in pregnant women and severe brain-based disorders in children could impact a generation with larger than usual numbers of members who have serious neurological difficulties.

    And without the resources of World Community Grid, using only the resources of our lab, we would only be able to screen a few thousand compounds against some of the Zika proteins, or it would take years to screen millions of compounds against all Zika proteins. This would severely limit our potential for drug discovery.

    Enlisting the help of World Community Grid volunteers will enable us to computationally evaluate over 20 million compounds in just the initial phase (and potentially up to 90 million compounds in future phases). Thus, running the OpenZika project on World Community Grid will allow us to greatly expand the scale of our project, and it will accelerate the rate at which we can obtain the results toward an antiviral drug for the Zika virus.

    By working together and sharing our work with the scientific community, many other researchers in the world will also be able to take promising molecular candidates forward, to accelerate progress towards defeating the Zika outbreak.

    *Science paper:
    Open drug discovery for the Zika virus [version 1; referees: 3 approved]

    **Science paper:
    Illustrating and homology modeling the proteins of the Zika virus [version 1; referees: 1 approved with reservations]

    See the full articles here and here.

    Please help promote STEM in your local schools.
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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 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-

    OpenZika

    Rutgers Open Zika
    Zika

    Help Stop TB
    WCG Help Stop TB
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    Outsmart Ebola Together

    Mapping Cancer Markers
    mappingcancermarkers2

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    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
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  • richardmitnick 8:37 pm on May 16, 2016 Permalink | Reply
    Tags: , Beyond Antibiotics, Medicine,   

    From NOVA: “Beyond Antibiotics” 

    PBS NOVA

    NOVA

    05 May 2016
    Jenny Morber
    Photo credits: Paenigenome/Wikipedia (CC BY-SA), Oxford Nanopore Technologies

    Late on the night of December 26, just three days after I had given birth to my son and two days after receiving two blood transfusions for complications, I was back in the hospital. This time, I had gone straight to the emergency room. There we were: me, my days-old baby, and my husband. The ER doctors put us in a separate room to try to isolate us from the contagion filling the hospital floor. But a few hours in, my husband started vomiting. He was asked to leave if he did not wish to become a patient. My baby could not stay with me. It was dangerous just having him there. I was alone.

    I had left the hospital with my baby on Christmas Day. As best I can recall, the discharge nurses had instructed me to call back if I developed a fever over 101˚ F. The day I checked into the ER, our thermometer had read just a few tenths of a degree over.

    The doctors knew I had recently been in the hospital, and they knew that I had lost a lot of blood. But they had no idea which bacterial strain was causing the fever, so they hedged their bets, giving me two different antibiotics—one for MRSA (methicillin-resistant Staphylococcus aureus), a common antibiotic-resistant strain of staph bacteria, and another antibiotic for the common infection culprit E. coli. When my hospital roommate heard I was on a drug for MRSA, she requested to be moved. I lay in bed alone, ordered hospital food, and pumped tainted breast milk.

    In the days that followed, I started eating ice in the hopes that it would trick the nurses’ thermometer and they would let me go home. I fooled no one. This low-grade fever would keep me in the hospital for twice as long as my massive blood loss did following birth.

    My two hospital stays illustrate how the script for medical care has flipped over the last several decades. In many ways, a hospital acquired infection has become more serious than an uncontrolled bleed. Bacteria and other pathogens are developing multi-drug resistance, and our last, best strategies are failing.

    You may have heard the rumblings. Doctors have been warned not to over-prescribe antibiotics. Consumers have been admonished against the antibacterial soaps and creams. We can now buy meat and dairy marked “animals not treated with antibiotics or hormones” in the supermarket. But those measures are only stop-gaps. They will only, perhaps, slow the pace of resistance.

    For years, researchers and doctors have known this. Responsible antibiotic use isn’t enough to win the pathogen war—it “reflects an alarming lack of respect for the incredible power of microbes,” wrote a group of infectious disease experts from across the U.S. in a 2008 “Call to Action” paper*. After all, they write, microbes have been evolving and adapting for 3.5 billion years. Thanks to their combination of genetic plasticity and rapid generation time—they can undergo as many as 500,000 generations during one of ours—they are especially good at overcoming evolutionary obstacles.

    Antibiotic resistance is just another byproduct of those abilities. It has evolved because patients don’t complete a full course of drugs or because animals receive drugs they don’t really need or because a college kid slathers his apartment in antibacterial spray. Antibiotics kill most but not all of the bacteria they encounter. The strongest ones live. These reproduce and pass on their advantages, and sometimes they get together and swap genes. Eventually, the resistant types grow very, very resistant.

    It wouldn’t be a problem if bacteria weren’t evolving resistance faster than we have been able to respond. New antibiotics are difficult to produce, and they don’t make as much profit as drugs for chronic disease, so there has been a dearth of investment. “Why it feels like it’s happening right now is that there aren’t really new antibiotics coming down the pipeline,” says Dr. Carmen Cordova, a microbiologist who works for the nonprofit National Resources Defense Council. “We don’t have really a plan B.”

    Three years ago, science journalist Maryn McKenna published an award-winning article in which she imagines a modern environment devoid of antibiotics. It’s a return to the medical dark ages in which illnesses like tuberculosis, pneumonia, and meningitis are death sentences. It would mean that burn victims, surgery patients, laboring mothers, and those undergoing chemotherapy would have to worry constantly about succumbing to infection.

    President Barack Obama has called antibiotic resistance “one of the most pressing public health issues facing the world today.” A conservative estimate from a British project called the Review on Antimicrobial Resistance states that, if left unchecked, antibiotic resistance will cause 10 million human deaths per year—more than the number of people who currently die from cancer and diabetes combined.

    The threat is looming. Late last year researchers identified bacteria resistant to a last-resort antibiotic in Chinese raw chicken and pork meat, slaughterhouse pigs, and hospital patients. The resistant gene has since been identified in bacteria across Asia and Europe.

    But we are fighting back. President Obama has asked Congress for $1.2 billion over five years for developing new diagnostic tools, creating a database of antibiotic resistant diseases, and funding research to better understand drug resistance. It joins other, ongoing efforts to identify promising new candidates. In labs and universities around the world, researchers are hard at work identifying, testing, and perfecting strategies that go well beyond what, today, we call antibiotics.
    Knocking Out Communications

    We used to think that bacteria were dumb. We thought they ate, pooped, divided, and not much else. We now know that this story is much too simple. Bacteria communicate, keep tabs on their environment, and respond and react. They ask how many others are around and how they are doing, and only when a certain number have congregated do most pathogenic bacteria turn virulent. The danger is in numbers.

    Of course, sometimes they gain the upper hand despite our best efforts. But what if there was a way to hide them from one another? What if we could shut down their party before it starts? That’s the idea behind quorum sensing inhibitors.

    1
    Paenibacillus vortex uses cell-to-cell communication to form colonies with complex shapes.

    Quorum sensing inhibitors (QSIs) are molecules designed to interfere with pathogen communication. When bacteria go looking for friends, they put out small molecules like little flags, saying, “I am here!” For the past two decades, researchers have been working to develop strategies that interfere with every step of the process, by halting production of these flags, obscuring them so that other bacteria cannot recognize them, or blocking responses when they are recognized.

    The results, so far, have been promising. According to Vipin Kalia, a researcher at the Institute of Genomics and Integrative Biology in Delhi India, such quorum sensing inhibitors are less likely to lead to bacterial resistance because, “Antibiotics create a pressure on bacteria because their survival is under threat. QSIs are not threatening their existence and survival.” Several of these inhibitors have been shown to reduce virulence in animals, Kalia says, and two have made it to clinical trials.

    Still, none are currently used to treat human diseases, and while it may be more difficult for bacteria to develop resistance to these inhibitors, it is not impossible. In fact, it may already be happening. In a 2014 paper in the journal Microbial Ecology, Kalia and his colleagues write that “evidence is accumulating that bacteria may develop resistance to QSIs.” It appears that communication is important enough to bacteria that they have several different channels. If one path is blocked, they try to use another. “Apparently” the researchers write, “bacteria do not even need to undergo any genetic change to withstand quorum sensing inhibitors.”

    QSIs may buy us some time, but will it be enough? Fortunately, there are other options.

    Creating an Inhospitable Environment

    The development of new antibiotics has often relied on tweaking existing drugs. It’s a simpler approach than developing an entirely new class of antibiotics, but the modifications are often small enough that bacteria can adapt relatively easily. Fortunately, plants, animals, fungi, and other microbes have been battling it out long before we arrived, and they have evolved a few good tricks.

    One, antimicrobial peptides (AMPs), were first identified in silk moths and are now known to be an innate immune response in almost all organisms from algae and plants to the entire animal kingdom. AMPs use differences between the membranes of a host cell and a bacteria to selectively target only the harmful microbe invader. Bacteria tend to be negatively charged, while mammalian cells tend to be neutral. The positively charged peptides glom onto the bacteria’s membrane and punch holes in it. Rather than having to recognize specific targets on the cell membrane, as traditional antibiotics do, AMPs grab any bacterial membrane that doesn’t belong and shoot it full of holes.

    AMPs happen to be much more resistant to bacterial adaptations. Despite their ancient origins, AMPs remain effective weapons today. “Bacteria can become resistant to antibiotics by simple modifications of the receptor where the drug attacks. To become resistant to AMPs…they need to change their entire membrane chemistry,” says Karen Lienkamp, a junior research group leader working on AMPs at the University of Freiburg in Germany.

    Right now, researchers are working on making materials that have synthetic versions of AMPs, or SAMPs, on the surface. These specially engineered surfaces help reduce microbe contamination on hospital equipment, in the air, and on clothing. Specifically, they prevent biofilms—clumps of bacteria that form protective nets around themselves. “Biofilms are the ‘root of all evil,’ ” Lienkamp says. “Studies with regular antibiotics have shown that you need up to 1,000 times the concentration to kill bacteria that are encapsulated in a biofilm.”

    Other strategies to prevent bacteria from taking up residence on hospital surfaces include extra-slippery materials and materials that shed layers to prevent buildup. Yet as promising as they are, anti-fouling surfaces are only useful for prevention. They won’t help someone who already has rampant infection. What we really need are ways to identify what ails us, and quickly, with customizable drugs to treat them.

    Faster Identification

    Justin O’Grady is a lecturer in medical microbiology at the University of East Anglia in the United Kingdom. Last year, he and others published a paper in the journal Nature Biotechnology about a technology that can take a sample of blood and, in six to eight hours, identify the bacteria that is causing an infection. In hospitals and labs today, it typically takes two to five days.

    The device is a gene sequencer called the MinION, which reads the bacteria’s genetic signature within minutes. It’s small enough to plug into a computer’s USB drive, and at around $1,000 for the necessary equipment, it doesn’t cost nearly as much as traditional laboratory-grade gene sequencers. Moreover, the device, when given another day or so to process the sample, can also identify which genes in an invading bacteria are responsible for the antibiotic resistance. “This would be a personalized medicine approach to antibiotic treatment,” O’Grady says.

    3
    A MinION sequencer.

    While other molecular identification technologies exist, sequencing technologies like the MinION are broad-spectrum microbe detectors. “The advantage of sequencing for this approach is that you get an unbiased diagnosis,” O’Grady says. “You don’t need to know anything about what pathogen might be in there.”

    If something like MinION had been available when I was in the hospital, my experience would probably have been quite different. It wouldn’t have taken doctors five days to determine the root cause, getting me home sooner and saving both the hospital and the insurance company a significant amount of money. I also would not have been administered ineffective antibiotics, preventing a small amount of evolved resistance.

    Instead of doctors treating their patients with best-guess antibiotics while they wait days for culture results to come back, sequencing technologies like these will tell them what is going on by the time the nurse comes around with the second dose. “If we can change the way that we prescribe antibiotics, we can improve antibiotic stewardship and we can improve patient management at the same time.” O’Grady says. “The patient receives better treatment quicker, and society benefits because we keep our potent antibiotics for those who need them most.”

    Building a Library

    The most promising new antibiotics may, counterintuitively, come from the bacterial domain itself. Though nature’s bacterial library could hold a multitude of undiscovered antibiotic recipes, sifting through its diversity is a daunting task: Most bacteria found in the environment—99%—will not grow on a petri dish in traditional cell culture.

    We may soon be able to unlock that library, though, thanks to the work of Kim Lewis, director of the Antimicrobial Discovery Center at Northeastern University in Boston. Lewis reported* last year in the journal Nature that he and his colleagues found a way to culture bacteria from the soil, which have been notoriously difficult to grow in the lab because they rely on signals and molecules from neighboring bacteria to grow.

    Lewis and his colleagues decided that rather than try to painstakingly recreate those conditions, they would just bring a little soil back to the lab. They started by collecting a small scoop of soil, rinsing it in water, mixing the water into culture medium, and then squirting the mixture into a device they developed called the iChip. They then placed the iChip into a bucket of the same soil kept in the lab. After a month they pulled the iChip out, cultured the bacteria, and observed what was growing. The bacteria were still growing in agar—not their ideal environment—but they were happier after the month spent back in the soil.

    “Ten percent of uncultured bacteria from the natural environment require growth factors from neighboring bacteria,” Lewis says. Their soil vacation seems to make the bacteria stronger, more adaptable, and more likely to grow on the iChip.

    Eager to build their library, Lewis and his colleagues began collecting from their back yards. If someone went on vacation, they were given a kit to bring back a sample. One collaborator took a serendipitous trip to Maine and returned with a completely new genus of bacteria, one that produced an incredibly effective antibiotic that kills other types of bacteria, which they named teixobactin. In experiments with human cells and in mice, teixobactin proved exceptionally effective at killing Clostridium difficile (a resistant bacteria that causes ulcers and is most effectively treated with fecal transplants) and Staphylococcus aureus, the bacteria whose resistant strains are called MRSA.

    Teixobactin must complete many hurdles before it can become a drug offered in the doctor’s office. It will need to be formulated to remain active inside the human body, toxicology tests will need to ensure that it does not confer nasty side effects, and experiments will need to determine other medicines it may interact with.

    Lewis is working with a company to improve the teixobactin’s solubility, and he estimates that it will take two years to get to clinical trials, which will then take at least another three years. So, even in the best case scenario, texiobactin will not be helping us to fight off antibiotic resistant disease for the next five years.

    In the Meantime

    Of course these are not the only promising technologies being developed to prevent, fight, and treat antibiotic resistant diseases. Bacteria-targeting viruses, gene editing, nanoparticles, and shotgun-like strategies using multiple drugs are all brimming with potential.

    But each of these needs time—time for research and development and optimization. In the meantime we will have to trust that our current technologies and common sense prevention provides the window we need. (Please, everyone, wash your hands.)

    As for my brush with an antibiotic-resistant infection, I eventually returned home to my husband and children. On the fifth day, lab results revealed why the drugs were not working. I did not have MRSA. I did have E. coli, but the strain I had was resistant to the drug they were giving me. Neither of the antibiotics was having any effect.

    The doctors had made their best guesses, but those guesses had been wrong. The hospital let me leave with new antibiotic and a tube inserted into a vein close to my heart. Don’t let that tube get dirty, they warned me, or the infection could kill you. Don’t get air in the line, they warned me, or that could kill you too.

    To say I was careful is an understatement. Three times a day I fed my newborn, put him down to sleep, and followed the hour-long procedure. Years of work in a nanotech laboratory had taught me how be meticulous. After two weeks, a nurse came and removed the line next to my heart. The treatment had worked. The bacteria I acquired at the hospital had not evolved resistance to every weapon in our arsenal. At least, not yet.

    *Science paper:
    The Epidemic of Antibiotic-Resistant Infections: A Call to Action for the Medical Community from the Infectious Diseases Society of America

    There are other science papers referenced in this article, but no links were provided. I have requested the links. I will update this post with whatever I get in the way of links.

    See the full article here .

    Please help promote STEM in your local schools.

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    NOVA is the highest rated science series on television and the most watched documentary series on public television. It is also one of television’s most acclaimed series, having won every major television award, most of them many times over.

     
  • richardmitnick 7:59 pm on May 16, 2016 Permalink | Reply
    Tags: , , Medicine, , Scientists Built a Giant Molecule That Could Fight Nearly Any Viral Infection   

    From NOVA: “Scientists Built a Giant Molecule That Could Fight Nearly Any Viral Infection” 

    PBS NOVA

    NOVA

    16 May 2016
    Allison Eck

    1
    Simian virus 40, a virus found in both monkeys and humans. No image credit.

    2
    The influenza virus. CDC/ Dr. Erskine. L. Palmer; Dr. M. L. Martin via Flickr

    Viruses have eluded our best efforts to fight them off. They mutate much more quickly than bacteria, and most anti-viral drugs that do keep symptoms at bay need to be administered for the rest of a patient’s life.

    But now, researchers may have discovered a workaround: a macromolecule that’s swift and nimble enough to tackle virtually any virus that crosses its path. The scientists, from both IBM and the Institute of Bioengineering and Nanotechnology in Singapore, recently published their findings* in the journal Macromolecules.

    The team concentrated their efforts on the similarities between viruses. Here’s Claire Maldarelli, writing for Popular Science:

    A group of researchers at IBM and the Institute of Bioengineering and Nanotechnology in Singapore sought to understand what makes all viruses alike.

    For their study, the researchers ignored the viruses’ RNA and DNA, which could be key areas to target, but because they change from virus to virus and also mutate, it’s very difficult to target them successfully.

    Instead, the researchers focused on glycoproteins, which sit on the outside of all viruses and attach to cells in the body, allowing the viruses to do their dirty work by infecting cells and making us sick. Using that knowledge, the researchers created a macromolecule, which is basically one giant molecule made of smaller subunits. This macromolecule has key factors that are crucial in fighting viruses. First, it’s able to attract viruses towards itself using electrostatic charges. Once the virus is close, the macromolecule attaches to the virus and makes the virus unable to attach to healthy cells. Then it neutralizes the virus’ acidity levels, which makes it less able to replicate.

    The researchers found that the molecules did in fact latch onto the a number of viruses’ glycoproteins (including those of the Ebola and dengue viruses) and reduced the number of viruses in their lab experiments. A sugar in the molecules was also able to bind to healthy immune cells that, in turn, destroyed the virus more efficiently.

    If the technique plays out as expected in further experiments, this lone molecule could someday be responsible for ridding humankind of the worst viral infections—from Ebola, to Zika, to the flu. That will take a while, though, and some scientists caution that universal antivirals may be dangerous, anyway—they could upset our immune systems in ways we don’t currently anticipate. Still, this macromolecule is a proof of concept that powerful antiviral drugs are not completely out of reach.

    *Science paper:
    Cooperative Orthogonal Macromolecular Assemblies with Broad Spectrum Antiviral Activity, High Selectivity, and Resistance Mitigation

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

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    NOVA is the highest rated science series on television and the most watched documentary series on public television. It is also one of television’s most acclaimed series, having won every major television award, most of them many times over.

     
  • richardmitnick 11:23 am on May 6, 2016 Permalink | Reply
    Tags: , , Medicine, Study suggests medical errors are third-leading cause of death in U.S.   

    From Hopkins: “Johns Hopkins study suggests medical errors are third-leading cause of death in U.S.” 

    Johns Hopkins
    Johns Hopkins University

    5.3.16
    Vanessa McMains

    Physicians advocate for changes in how deaths are reported

    1

    Analyzing medical death rate data over an eight-year period, Johns Hopkins patient safety experts have calculated that more than 250,000 deaths per year are due to medical error in the U.S. Their figure, published May 3 in The BMJ, surpasses the U.S. Centers for Disease Control and Prevention’s third leading cause of death—respiratory disease, which kills close to 150,000 people per year.

    The Johns Hopkins team says the CDC’s way of collecting national health statistics fails to classify medical errors separately on the death certificate. The researchers are advocating for updated criteria for classifying deaths on death certificates.

    “Incidence rates for deaths directly attributable to medical care gone awry haven’t been recognized in any standardized method for collecting national statistics,” says Martin Makary, professor of surgery at the Johns Hopkins University School of Medicine and an authority on health reform. “The medical coding system was designed to maximize billing for physician services, not to collect national health statistics, as it is currently being used.”

    In 1949, Makary says, the U.S. adopted an international form that used International Classification of Diseases billing codes to tally causes of death.

    “At that time, it was under-recognized that diagnostic errors, medical mistakes, and the absence of safety nets could result in someone’s death,” says Makary, “and because of that, medical errors were unintentionally excluded from national health statistics.”

    In their study, the researchers examined four separate studies that analyzed medical death rate data from 2000 to 2008. Then, using hospital admission rates from 2013, they extrapolated that based on a total of 35,416,020 hospitalizations, 251,454 deaths stemmed from a medical error, which the researchers say now translates to 9.5 percent of all deaths each year in the U.S.

    According to the CDC, in 2013, 611,105 people died of heart disease, 584,881 died of cancer, and 149,205 died of chronic respiratory disease—the top three causes of death in the U.S. The newly calculated figure for medical errors puts this cause of death behind cancer but ahead of respiratory disease.

    “Top-ranked causes of death as reported by the CDC inform our country’s research funding and public health priorities,” Makary says. “Right now, cancer and heart disease get a ton of attention, but since medical errors don’t appear on the list, the problem doesn’t get the funding and attention it deserves.”

    The researchers caution that most medical errors aren’t due to inherently bad doctors, and that reporting these errors shouldn’t be addressed by punishment or legal action. Rather, they say, most errors represent systemic problems, including poorly coordinated care, fragmented insurance networks, the absence or underuse of safety nets, and other protocols, in addition to unwarranted variation in physician practice patterns that lack accountability.

    “Unwarranted variation is endemic in health care,” Makary says. “Developing consensus protocols that streamline the delivery of medicine and reduce variability can improve quality and lower costs in health care. More research on preventing medical errors from occurring is needed to address the problem.”

    See the full article here .

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    Johns Hopkins Campus

    The Johns Hopkins University opened in 1876, with the inauguration of its first president, Daniel Coit Gilman. “What are we aiming at?” Gilman asked in his installation address. “The encouragement of research … and the advancement of individual scholars, who by their excellence will advance the sciences they pursue, and the society where they dwell.”

    The mission laid out by Gilman remains the university’s mission today, summed up in a simple but powerful restatement of Gilman’s own words: “Knowledge for the world.”

    What Gilman created was a research university, dedicated to advancing both students’ knowledge and the state of human knowledge through research and scholarship. Gilman believed that teaching and research are interdependent, that success in one depends on success in the other. A modern university, he believed, must do both well. The realization of Gilman’s philosophy at Johns Hopkins, and at other institutions that later attracted Johns Hopkins-trained scholars, revolutionized higher education in America, leading to the research university system as it exists today.

     
  • richardmitnick 2:45 pm on May 3, 2016 Permalink | Reply
    Tags: , Columbia University Medical Center, Hi-Res Images Reveal How a “SuperBug” Hides from Antibiotics, Medicine   

    From Columbia: “Hi-Res Images Reveal How a “SuperBug” Hides from Antibiotics” 

    Columbia U bloc

    Columbia University

    CUMC bloc

    March 7, 2016 [just appeared in social media]

    1
    Multidrug-resistant Klebsiella pneumoniae gram-negative bacteria are known to cause severe hospital-acquired infections. Image: David Dorward, PhD, National Institute of Allergy and Infectious Diseases

    “The force” is not just for Jedi knights.

    Bacteria have developed their own “force” to hide from our antibiotics, and they are increasingly using this strategy to chip away at the effectiveness of polymyxins, our last line of defense against some “superbug” infections.

    Biologists at Columbia are now peering inside these bacteria with super high-resolution imaging techniques and have found places where drugs could disrupt the bugs’ defense and restore their susceptibility to these powerful antibiotics.

    To evade detection by polymyxin antibiotics, bugs like E. coli, Salmonella, and Klebsiella pneumoniae–all gram-negative bacteria–are known to alter their electrostatic charge.

    “Polymyxins find bacteria via electrostatic attraction,” says Vasileios Petrou, PhD, a postdoc in the lab of Filippo Mancia, PhD, assistant professor of physiology & cellular biophysics. “Polymyxins are positively charged, so they are attracted to negatively charged parts of the bacteria.”

    Bacteria become resistant to polymyxins by placing a cap, made from a sugar molecule, over the negative charge. This trick alters the electrostatic forces between the bacteria and antibiotics.

    “It’s like the bacteria become invisible to polymyxins,” Dr. Mancia says. “The antibiotics can’t stick to the bacteria or kill them.”

    An enzyme called ArnT in the membrane of these bacteria is responsible for the capping. First, ArnT grabs a sugar from a lipid, then the sugar is planted on the negative charge.


    Access mp4 video here .

    The Columbia researchers were able to visualize the precise details of this process by using X-ray crystallography to reveal the location of each individual atom in the ArnT enzyme before and after it grabs the sugar [see video above].

    These images reveal places where the enzyme could be disabled. “To grab the sugar, the ArnT enzyme must first bind to the lipid that carries it, and this binding happens in a large ‘pocket’ in the enzyme’s side,” says Jérémie Vendome, PhD, a research associate scientist in the lab of Barry Hönig.

    Filling the pocket with a drug could prevent the binding. “Essentially, that would sensitize the bacteria to the antibiotic again,” Dr, Petrou says.

    Dr. Vendome is now using computerized techniques to virtually screen millions of potential drug candidates to detect those that fit in the pocket. Hits generated from the virtual screening will be tested with polymyxins to see if the combination can eliminate antibiotic-resistant bacteria.

    “We are not pharma, but we can do some initial development in the lab,” Dr. Mancia says. “We hope that this work will lead to the development of a co-drug that will allow us to extend the lives of already available antibiotics.”

    Details of the research were published* Feb. 5 in the journal Science.

    The research performed at Columbia University was supported by grants from the NIH (U54GM095315, R01GM111980) and a Charles H. Revson Senior Fellowship. The New York Consortium on Membrane Protein Structure, led by Wayne Hendrickson, PhD, contributed valuable support.

    *Science paper:
    Structures of aminoarabinose transferase ArnT suggest a molecular basis for lipid A glycosylation

    See the full article here .

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    Columbia U Campus

    Columbia University was founded in 1754 as King’s College by royal charter of King George II of England. It is the oldest institution of higher learning in the state of New York and the fifth oldest in the United States.

     
  • 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
    ibm

    IBM – Smarter Planet
    sp

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

     
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