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  • richardmitnick 12:23 pm on November 25, 2015 Permalink | Reply
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    From U Washington: “New center seeks therapies to boost body’s immune system” 

    U Washington

    University of Washington

    Bobbi Nodell

    Research on immune responses underway at a UW Department of Immunology lab. Dennis Wise

    A new Center for Innate Immunity and Immune Disease at UW Medicine seeks to become a world leader in finding therapies to regulate the body’s defense system and fend off a wide variety of diseases. Among these are infectious illnesses like Ebola, influenza and dengue fever, autoimmune disorders like rheumatoid arthritis, multiple sclerosis and lupus, and common, complex conditions, like cancer, diabetes and cardiovascular disease.

    The research center, which was formed over the past two years, will officially open for business in January. A seminar and reception to introduce the center will be held at 3:30 p.m., Monday, Nov. 30, at UW Medicine South Lake Union, Building E, 750 Republican St., Seattle.

    Michael Gale Jr., University of Washington professor of immunology and director of the new center, will provide an overview at the event; his talk will stream live.

    Dr. Gale sat down to answer a few question about the center’s goal to “harness the immune system,” the second most complex system in the body next to the brain:

    Q. What does it mean to harness the immune system?

    A. Our bodies have an inborn ability to respond to infections. It doesn’t require pre-exposure. This response is called the innate immune response. Depending on how the innate response plays out, the rest of the immune response will follow – whether it’s going to activate a T-cell to attack a cancer cell or to turn against our own body, for example. The innate immune response shapes the overall immune response. Scientists didn’t know that five to eight years ago. We are studying innate immunity to the point we can harness these processes to enhance or control the immune response.

    Q. Why Seattle?

    A. Seattle is a hotbed for this kind of research. We now have a critical mass of expertise to support a center like this. UW Medicine has one of the highest-ranking immunology departments in the world. Great research institutions, such as Benaroya Research Institute, Fred Hutchinson Cancer Research Center, Institute for Systems Biology, Center for Infectious Disease Research, and Seattle Children’s Research Institute are all in walking distance.

    These institutions, as well as several local biotech companies, have people working on being able to trigger an immune system response for various diseases, but there isn’t one center coordinating all the activity and providing the infrastructure.

    Q. What will the Center for Innate Immunity and Immune Disease offer?

    A. We will be the place coordinating different research efforts in innate immunity to push discoveries into human therapies.

    Researchers working in an immunology lab at UW Medicine South Lake Union.

    With local biotech partners, scientists can quickly test and develop these new advances toward clinical applications.

    We have already discovered drug targets and drug-like compounds of innate immune regulation. These research findings offer the promise to treat Ebola virus, influenza, and West Nile virus infections. The center will help bring forward similar discoveries in autoimmune disease, inflammatory disease and cancer.

    Q. Who will be involved in the center?

    A. The center will have scientists from different fields of expertise, such as infectious disease, rheumatology, computational biology, protein biology, pharmaceutics, vaccinology, genetics, and pathology, microbiology, immunology, and medicine, as well as industry partners. They will work with clinicians to bring understanding from diverse perspectives and with our biotech partners and others to evaluate whether a therapy is ready for preclinical and clinical development.

    Q. What is one of the leading edge technologies used by the center?

    A. The center will be designed around four service cores – cell signaling, transgenic mouse models, immunoinformatics, and translational research. It will also have an educational outreach core. All the cores are innovative, but probably the most cutting edge is the immunoinformatics core. It brings together a group of computational biologists who can process high throughput data sets and build computational models to help steer the research direction. [High throughput is the running of several experimental test simultaneously.]

    Q. What kind of outreach does the center do?

    A. The education outreach core is looking at the next generation by bringing basic immunology teaching and lab exercises in immunology to local public school students. This core also runs a summer research internship in its members’ labs for high school students.

    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.

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  • richardmitnick 12:58 pm on November 10, 2015 Permalink | Reply
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    From TUM: “Possible Reasons Found for Failure of Alzheimer’s Treatment” 

    Techniche Universitat Munchen

    Techniche Universitat Munchen

    Dr. Vera Siegler

    High-resolution two-photon microscopy: Pictures of cells (green) and amyloid-β plaques (blue) in Alzheimer’s brain. (Picture: Marc Aurel Busche / TUM)

    Agglutinated proteins in the brain, known as amyloid-β plaques, are a key characteristic of Alzheimer’s. One treatment option uses special antibodies to break down these plaques. This approach yielded good results in the animal model, but for reasons that are not yet clear, it has so far been unsuccessful in patient studies. Scientists at the Technical University of Munich (TUM) have now discovered one possible cause: they noticed that, in mice that received one antibody treatment, nerve cell disorders did not improve and were even exacerbated.

    Immunotherapies with antibodies that target amyloid-β were long considered promising for treating Alzheimer’s. Experiments with animals showed that they reduced plaques and reversed memory loss. In clinical studies on patients, however, it has not yet been possible to confirm these results. A team of researchers working with Dr. Dr. Marc Aurel Busche, a scientist at the TUM hospital Klinikum rechts der Isar Klinik und Poliklinik für Psychiatrie und Psychotherapie and at the TUM Institute of Neuroscience, and Prof. Arthur Konnerth from the Institute of Neuroscience has now clarified one possible reason for this. The findings were published in Nature Neuroscience.

    Immunotherapy Increases Number of Hyperactive Nerve Cells

    The researchers used Alzheimer’s mice models for their study. These animals carry a transgene for the amyloid-β precursor protein, which, as in humans, leads to the formation of amyloid-β plaques in the brain and causes memory disorders. The scientists treated the animals with immunotherapy antibodies and then analyzed nerve cell activity using high-resolution two-photon microscopy. They found that, while the plaques disappeared, the number of abnormally hyperactive neurons rose sharply.

    “Hyperactive neurons can no longer perform their normal functions and, after some time, wear themselves out. They then fall silent and, later, possibly die off,” says Busche, explaining the significance of their discovery. “This could explain why patients who received the immunotherapy experienced no real improvement in their condition despite the decrease in plaques,” he adds.

    Released Oligomers Potential Reason for Hyperactivity

    Even in young Alzheimer’s mice, when no plaques were yet detectable in the brain, the antibody treatment led to increased development of hyperactive nerve cells. “Looking at these findings, even using the examined immunotherapies at an early stage, before the plaques appear, would offer little chance of success. As the scientist explains, the treatment already exhibits these side effects here, too.

    “We suspect that the mechanism is as follows: The antibodies used in treatment release increasing numbers of soluble oligomers. These are precursors of the plaques and have been considered problematic for some time now. This could cause the increase in hyperactivity,” says Busche.

    The work was funded by an Advanced ERC grant to Prof. Arthur Konnerth, the EU FP7 program (Project Corticonic) and the Deutsche Forschungsgemeinschaft (IRTG 1373 and SFB870). Marc Aurel Busche was supported by the Hans und Klementia Langmatz Stiftung.

    Marc Aurel Busche, Christine Grienberger, Aylin D. Keskin, Beomjong Song, Ulf Neumann, Matthias Staufenbiel, Hans Förstl and Arthur Konnerth, Decreased amyloid-β and increased neuronal hyperactivity by immunotherapy in Alzheimer’s models, Nature Neuroscience, November 9, 2015.
    DOI: 10.1038/nn.4163

    See the full article here .

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    Techniche Universitat Munchin Campus

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

  • richardmitnick 12:04 pm on November 10, 2015 Permalink | Reply
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    From New Scientist: “Ultrasound prises open brain’s protective barrier for first time” 


    New Scientist

    10 November 2015
    Helen Thomson


    For the first time, the barrier that protects the brain has been opened without damaging it, to deliver chemotherapy drugs to a tumour.

    The breakthrough could be used to treat pernicious brain diseases such as cancer, Parkinson’s and Alzheimer’s, by allowing drugs to pass into the brain.

    The blood-brain barrier keeps toxins in the bloodstream away from the brain. It consists of a tightly packed layer of endothelial cells that wrap around every blood vessel throughout the brain. It prevents the passage of viruses, bacteria and other toxins, while ushering in vital molecules such as glucose via specialised transport mechanisms.

    The downside of this is that the blood-brain barrier also blocks the vast majority of drugs. There are a few exceptions, but those drugs that are able to sneak through can also penetrate every cell in the body, which makes for major side effects.

    Now researchers at Sunnybrook Health Sciences Centre in Toronto, Canada, say they have successfully used ultrasound to temporarily open the blood-brain barrier, with the ultimate aim of treating a brain tumour. The procedure took place on 4 November.


    The team, led by neurosurgeon Todd Mainprize and physicist Kullervo Hynynen, injected the chemotherapy drug doxorubicin along with tiny gas-filled microbubbles, into the blood of a patient with a brain tumour. The microbubbles and the drug spread throughout their body, including into the blood vessels that serve the brain.

    Next the team applied focused ultrasound to the tumour and surrounding tissue via a cap full of transducers. The high-intensity ultrasound waves directed into the brain caused the microbubbles to vibrate.

    The vibrating bubbles expanded and contracted about 200,000 times a second, forcing apart the endothelial cells that form the blood-brain barrier. The idea is that this would allow doxorubicin in the bloodstream to sneak through the gaps in the barrier and into nearby tumour cells.

    The team confirmed that the blood-brain barrier had been breached by injecting a harmless contrast agent called gadolinium into the patient. Gadolinium cannot normally cross the barrier, says Mainprize. However, MRI scans clearly showed that the areas disrupted by the ultrasound contained gadolinium after the treatment, demonstrating that the blood-brain barrier had opened, he says.

    A day later, the patient received traditional surgery to remove the tumour. The team will analyse the tissue to calculate how much of the drug reached its intended target. The patient is the first of 10 people who will receive the treatment, before the team publishes its results.

    The team announced their breakthrough today at a virtual press conference.

    “Opening the barrier is really of huge importance. It is probably the major limitation for innovative drug development for neurosciences,” said Bart De Strooper, co-director of the Leuven Institute for Neuroscience and Disease in Belgium, when the trial was launched.

    Images credit: Sunnybrook/Doug Nicholson/MediaSource

    See the full article here .

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  • richardmitnick 2:38 pm on November 9, 2015 Permalink | Reply
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    From Brown: “After beating it, student gymnast takes fight to MRSA with research” 

    Brown University
    Brown University

    November 9, 2015
    David Orenstein


    Athletes are at elevated risk.Having beaten the “superbug,” Tori Kinamon now has methicillin-resistant Staphylococcus aureus squarely in her sights. She hopes her research will lead to strategies for reducing the risk of infection. Photos: Stew Milne for Brown University

    Toward the end of her month-long stay in Rhode Island Hospital, as she began to recover from eight surgeries on her left leg in two weeks, Tori Kinamon of Peachtree City, Ga., was up on crutches, trying out a stairwell where a window faced northeast.

    “I remember looking out and seeing the Sci Li across the way and the reality of my experience really hit me at that moment,” she said. “I remember thinking, ‘That’s where I should be right now. I should be in the Sci Li studying or just be on Brown’s campus and instead I’m here.’ That was a really hard reality to face.”

    This was not the way Kinamon wanted to spend the early spring of her freshman year in 2014. Instead of finishing her first season with the Brown gymnastics team and continuing her studies, she was battling an overwhelmingly painful infection of methicillin-resistant Staphylococcus aureus [MRSA]. At its peak the infection seriously threatened to take her leg, if not her life.

    In the end, the so-called “superbug” took a lot of muscle and left a two-foot long scar, but last spring Kinamon was back up on the uneven bars in competition for her team and her school. She had made the decision that MRSA wasn’t going to chase her out of the gym. Gymnastics is the closest thing to flying, she said, and after competing as an individual throughout high school she was indelibly excited to be part of a team at Brown.

    Kinamon managed to finish her freshman year courses from home early that summer, but it would take much longer to rebuild the lost muscle to competition strength. She had a lingering fear that somehow she could become infected again, but she had the drive, the faith, and the support of her team and family to fly again.

    “I didn’t just want to be able to walk, I wanted to be able to run and jump and return to my previous fitness level,” she said. “I didn’t want the MRSA infection to define what I did.”

    A broader perspective “It’s enabled me to explore how I can translate my experience into something that helps others avoid this preventable infection.

    In the best way, though, that’s only half-true. While she has defied MRSA by competing again athletically (winning the Mari-Rae Sopper Spirit Award from USA Gymnastics in April), she has made MRSA a defining aspect of her academic life. She didn’t just fend off the bacterium. As a Brown student, she’s now coming after it.

    Resurgent with research

    This semester the health and human biology concentrator is taking classes on the epidemiology of infectious diseases, immunology, and the burden of disease in developing nations. But all year she’ll also be working in the lab of Dr. Eleftherios Mylonakis, the Dean’s Professor of Medical Science and chief of infectious diseases at Rhode Island Hospital and The Miriam Hospital.

    Her focus is on finding out how to prevent MRSA from spreading. A lot of research has explored control within hospitals, but far less can explain how it manages to afflict healthy people in the community. Athletes are at elevated risk. Last month, MRSA ended the football season for New York Giants tight end Daniel Fells.

    As in Fells’ case, Kinamon doesn’t know how she got the terrible bacteria, but she wants to find out. She started her research this fall by undertaking a detailed review of the scientific literature on MRSA cases in athletes. She’s studying prevention practices, such as screenings, and information on how infections occur.

    “Right now I’m looking at the prevalence of MRSA colonization in athletes to see if it is known, and if it is known, how do we go about decolonizing people to reduce the risk of transmission to others in the community,” she said. “I hope that will extend to some lab work in looking at specifics of the [particularly virulent] community-acquired MRSA strains.”

    Mylonakis praised Kinamon as “analytical, supremely motivated, meticulous and scientifically curious.” Her personal story has been inspiring for his research group, he said, and her work will add to the scope of what it can accomplish.

    “This work will highlight that everyone — even young individuals at the best shape of their lives — is potentially vulnerable to these resistant pathogens and has already generated scientific questions on the molecular pathogenesis of MRSA that Tori is planning to investigate in the lab,” he said. “Her work has summarized what we know about the spread of MRSA among athletes. More importantly, it demonstrates a lot of missing links that will need to be studied. I anticipate that Tori’s work will be instrumental in developing prophylaxis strategies among athletes.”

    A patient’s perspective

    Doing all this in her junior year gives Kinamon an opportunity to explore more about infectious disease overseas next year. Originally she came to Brown hoping to prepare for medical school with a focus on sports medicine. That remains an interest, but after her ordeal she’s broadened her perspective to pursue a concentration subfocus in global and international health. She’s had the guidance of professors such as Mylonakis, Dr. Tim Flanigan, professor of medicine, and Katherine Smith, associate dean of biology for undergraduate education, but she also took to heart what someone said, perhaps off-handedly, while she was in the hospital.

    “Someone said to me, ‘You’re really lucky you are not in a Third-World country,’” she said. “That made me very interested in why, if someone had a MRSA infection in another country, their outcome could have been totally different just based on the resources they have.”

    Kinamon said being a patient, and not just a student, has changed how she looks at her studies and her future career.

    “When I was hospitalized, my eyes were suddenly and unexpectedly opened to the patient aspect of medicine,” she said. “The experience has allowed me to empathize with people in ways that I couldn’t have before.”

    As much pain and fear as she felt, as hard as she’s had to work, she has come through it with sense of what she gained, rather than what she lost.

    “Looking back on my experience, I wouldn’t change what happened to me because it’s completely altered the way I look not only at the world but also at myself,” she said. “Through Brown’s open curriculum and the breadth of opportunities available, I’ve been able to tailor my educational experience so that I can really look into what happened to me and why it happened. More importantly, it’s enabled me to explore how I can translate my experience into something that helps others avoid this preventable infection.”

    She wouldn’t change her experience, but she might change the game, squashing a superbug as she sticks what once may have seemed to be an impossible landing.

    See the full article here .

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    Welcome to Brown

    Brown U Robinson Hall
    Located in historic Providence, Rhode Island and founded in 1764, Brown University is the seventh-oldest college in the United States. Brown is an independent, coeducational Ivy League institution comprising undergraduate and graduate programs, plus the Alpert Medical School, School of Public Health, School of Engineering, and the School of Professional Studies.

    With its talented and motivated student body and accomplished faculty, Brown is a leading research university that maintains a particular commitment to exceptional undergraduate instruction.

    Brown’s vibrant, diverse community consists of 6,000 undergraduates, 2,000 graduate students, 400 medical school students, more than 5,000 summer, visiting and online students, and nearly 700 faculty members. Brown students come from all 50 states and more than 100 countries.

    Undergraduates pursue bachelor’s degrees in more than 70 concentrations, ranging from Egyptology to cognitive neuroscience. Anything’s possible at Brown—the university’s commitment to undergraduate freedom means students must take responsibility as architects of their courses of study.

  • richardmitnick 6:45 am on November 5, 2015 Permalink | Reply
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    From MIT Tech Review: “New Sepsis Detector Shrinks the Diagnosis from Days to Hours” 

    MIT Technology Review
    M.I.T Technology Review

    November 4, 2015
    Mike Orcutt

    A new FDA-approved diagnostic test can detect sepsis-causing pathogens directly from a blood sample.T2 Biosystems

    Sepsis affects more than a million people every year in the U.S. alone, and diagnosis can take five days. A new tool cuts the time to five hours.

    Hospitals are beginning to use a new, more potent weapon against sepsis, the devastating condition that kills more than 25 percent its victims and costs hospitals billions of dollars annually. In the U.S. alone, more than a million people become infected each year, and it contributes to as many half of all deaths in hospitals.

    Last fall, the U.S. Food and Drug Administration approved the new technology, developed by T2 Biosystems, for diagnosing sepsis caused by a fungus called Candida, the predominant cause of fungal sepsis. Several hospitals have begun deploying T2’s Candida-detection system, which is based on the same physical principle behind magnetic resonance imaging. By the end of this year the company aims to have 30 hospitals signed on to purchase and use the technology.

    Sepsis is a destructive reaction to an infection marked by an overwhelming inflammatory response throughout the body. If left untreated, sepsis can cause organ malfunction and death. Treating a septic patient requires pinpointing the bacterial or fungal organism that is the root cause. Today that process takes at least a day, and can take up to five days, as the patient’s condition worsens. T2 Biosystems says its novel pathogen detector, called T2 Magnetic Resonance (T2MR), can identify the bug within five hours.

    Doctors typically give a septic patient an immediate dose of a so-called broad-spectrum antibiotic that kills a variety of different bacteria, and then try to figure out the specific bug at fault by drawing blood and performing a lab test called a blood culture. At that point it is a race against the unidentified pathogen, and the blood culture step, which often doesn’t work, simply takes too long, says T2 Biosystems CEO John McDonough. McDonough cites clinical data that implies that if patients can get the right drug within 12 hours of first showing symptoms, the chance of death can be cut in half. “Every hour of delayed therapy increases mortality by 7 to 8 percent,” he says.

    Broad-spectrum antibiotics often don’t work, and are useless against fungal sepsis, which is even more deadly than bacterial sepsis. Candida infections in the bloodstream kill some 40 percent of patients.

    “We have the only technology we’re aware of that can go directly from a blood sample to a species-specific diagnostic test result,” says McDonough. It’s also more accurate than a blood culture. In a recent head-to-head comparison involving 55 patients known to have Candida infections, T2MR detected the pathogen in 96 percent of the patients, whereas blood culture detected it in only 60 percent.

    The T2MR detector works by measuring changes in the magnetic properties of the water molecules in the sample. After some processing steps, magnetic nanoparticles, equipped on their surface with strands of DNA complementary to strands in the target pathogen, are mixed with the sample. If a given target is present, the particles will attach to it and cluster, causing changes in the magnetic properties of the water molecules in the sample. Applying magnetic pulses elicits a response from those molecules, called T2 relaxation, and by measuring the change in this signal, the device automatically determines whether or not a given bug is present.

    Six hospitals have begun using T2’s Candida diagnostic test, and 13 more have signed contracts to adopt the technology. Next in the pipeline is a bacteria detector aimed at the bugs not covered by broad-spectrum antibiotics. The company expects to begin testing the bacteria detector in clinical trials early next year. If it can get FDA-approval for this test as quickly as it did for the Candida test, the bacteria diagnostic could be in the market as early as 2017.

    See the full article here .

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  • richardmitnick 6:32 am on October 29, 2015 Permalink | Reply
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    From EPFL: “When false alarms pollute intensive care” 

    EPFL bloc

    Ecole Polytechnique Federale Lausanne

    Sandy Evangelista

    Alain Herzog EPFL

    Two EPFL doctoral students created algorithms capable of eliminating false alarms that pollute intensive care units. To do this, they came up with the idea of pairing electrocardiogram data with optical waveform data. Their work has won top honors at the Computing in Cardiology conference at MIT.

    Intensive care units are known for their incessant symphony of alerts. 90% of them are false alarms, and they are so common that medical staff no longer pay them much heed. These false alarms are the result of several factors, such as when electrodes placed on the patient move, causing artifacts that trigger an alert. The alerts stream forth, filling the air day and night. They have a negative impact on both patients and medical staff: they disrupt the patients’ sleep, but, more importantly, they cause alarm fatigue among staff.

    This very topic – reducing false arrhythmia alarms in the ICU – was the focus of the 2015 Computing in Cardiology conference. This annual conference, organized in conjunction with MIT, features a competition involving the application of computers in the area of cardiology in order to improve patient care. Sibylle Fallet and Sasan Yazdani, PhD students at EPFL’s Applied Signal Processing Group (ASPG), took up this year’s challenge. The approach they developed, which cut the number of false alarms in half, earned them first place in the competition.

    Bradycardia, tachycardia, asystole, arrhythmia, fibrillation – the two EPFL doctoral students had to quickly master the medical jargon since their research focused on signal analysis in cardiology. “This challenge was right in line with their respective projects,” said Jean-Marc Vesin, Senior Scientist at the ASPG. “Sybille is working on an algorithm for instantaneous estimation that will, among other things, help in monitoring the vital functions of premature babies, and Sasan developed an algorithm capable of reliably detecting R wave peaks in ECGs, something that will improve sensors embedded in smart clothes, for example.”

    Sinus bradycardia seen in lead II with a heart rate of about 50.

    ECG showing sinus tachycardia with a rate of about 100 beats per minute

    A rhythm strip showing two beats of normal sinus rhythm followed by an atrial beat and asystole.

    Ventricular fibrillation (VF) an example of a serious cardiac arrhythmia.

    Like all the other competitors, the EPFL students were given the electrocardiograms of 1,250 patients. “We were provided with different signals. Even if they weren’t always high quality, most of the time we had the ECG and visual data from the PPG, which is read by placing a sensor on the patient’s finger,” said Sibylle. The PPG – short for photoplethysmograph – uses light absorption technology to detect waves produced by the body’s pulse.

    The real hurdle in this type of exercise is to precisely measure the heart rate. Because the quality of the signals can vary, catching each beat is no mean feat. The two algorithms developed by Sibylle and Sasan pick up where the other leaves off. If electrical activity does not show up clearly on the electrocardiogram, the photoplethysmographic waveform can provide the missing data.

    “Thanks to this dual monitoring, we eliminated 87% of the false alarms while effectively detecting real alerts,” said Sibylle.
    “When we were working on this we kept in mind that it could be attached to real intensive-care monitors, so most of our algorithms work in real time and don’t require much memory to do the calculations,” said Sasan.

    The researchers will publish an article in an upcoming issue of Physiological Measurement. Sibylle Fallet and Sasan Yazdani’s work was carried out under the Nano-Tera initiative, which is funded by the Swiss government.

    See the full article here .

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    EPFL is Europe’s most cosmopolitan technical university. It receives students, professors and staff from over 120 nationalities. With both a Swiss and international calling, it is therefore guided by a constant wish to open up; its missions of teaching, research and partnership impact various circles: universities and engineering schools, developing and emerging countries, secondary schools and gymnasiums, industry and economy, political circles and the general public.

  • richardmitnick 10:22 am on October 26, 2015 Permalink | Reply
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    From EPFL: “Monitoring critical blood levels in real time in the ICU” 

    EPFL bloc

    Ecole Polytechnique Federale Lausanne

    Emmanuel Barraud

    The biosensor and the app aimed at monitoring the results in real time. Alain Herzog/ EPFL 2015

    For patients in intensive care, knowing how much glucose, lactate and other substances are in the blood is a question of life or death. EPFL has developed a miniaturized microfluidic device that will allow medical staff to monitor these levels in real time and react more quickly. It was unveiled yesterday in Atlanta.

    No larger than a pack of chewing gum, the prototype developed by EPFL’s Integrated Systems Laboratory (LSI) is deceptively simple in appearance. But this little black case with two thin tubes sticking out contains some real miniaturized high-tech wonders. “We embedded biosensors in it to measure several different substances in the blood or blood serum along with an array of electronics to transmit the results in real time to a tablet via Bluetooth,” said Sandro Carrara, an LSI scientist.

    Capable of being connected to a drainage tube that’s already in place, the new system is much less invasive than the many monitoring devices that it’s designed to replace. It keeps constant tabs on the blood levels of five substances: metabolites (glucose, lactate and bilirubin) and ions (calcium and potassium), all of which indicate changes in the condition of intensive-care patients.

    “Nowadays, several of these levels are measured periodically. But in some cases, any change in level calls for an immediate response, something that is not possible with the existing systems,” said Dr. Carrara.

    Freeing space around the patient

    Building on this principle, up to 40 molecules could be monitored in real time. This advance will drastically reduce the number of machines cluttered around patients – an obvious practical advantage for the medical staff, not to mention the psychological boon for loved ones.

    The prototype, which was made with a 3D printer, has been successfully tested on rodents. Discussions are now under way for tests to be carried out at the University Hospital of Lausanne (CHUV). And a number of manufacturers have already expressed serious interest in developing this device. “We could hit the market in two to three years,” said Dr. Carrara.

    This progress towards more precise and effective medicine was achieved under the Nano-Tera initiative, which is financed by the Swiss government. The device was unveiled yesterday in Atlanta at the 2015 BioCAS Conference.

    See the full article here .

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    EPFL is Europe’s most cosmopolitan technical university. It receives students, professors and staff from over 120 nationalities. With both a Swiss and international calling, it is therefore guided by a constant wish to open up; its missions of teaching, research and partnership impact various circles: universities and engineering schools, developing and emerging countries, secondary schools and gymnasiums, industry and economy, political circles and the general public.

  • richardmitnick 8:28 am on October 26, 2015 Permalink | Reply
    Tags: , Medicine, , Snake venom   

    From Rice: “Snake venom helps hydrogels stop the bleeding” 

    Rice U bloc

    Rice University

    October 26, 2015
    Mike Williams

    Rice University researchers Jeffrey Hartgerink, left, and Vivek Kumar led research that combines a derivative of snake venom with their nanofiber hydrogel to help encourage blood clotting in wounds, even for patients who take anti-coagulant medications. (Credit: Jeff Fitlow/Rice University)

    The Brazilian lancehead is one of several South American pit vipers that produce venom that has proven to be a powerful blood coagulant. Scientists at Rice University have combined a derivative of the venom with their injectable hydrogels to create a material that can quickly stop bleeding and protect wounds, even in patients who take anti-coagulant medications. (Credit: Photo by Greg Hume via Wikipedia)

    A nanofiber hydrogel infused with snake venom may be the best material to stop bleeding quickly, according to Rice University scientists.

    The hydrogel called SB50 incorporates batroxobin, a venom produced by two species of South American pit viper. It can be injected as a liquid and quickly turns into a gel that conforms to the site of a wound, keeping it closed, and promotes clotting within seconds.

    Rice chemist Jeffrey Hartgerink, lead author Vivek Kumar and their colleagues reported their discovery in the American Chemical Society journal ACS Biomaterials Science and Engineering. The hydrogel may be most useful for surgeries, particularly for patients who take anti-coagulant drugs to thin their blood.

    “It’s interesting that you can take something so deadly and turn it into something that has the potential to save lives,” Hartgerink said.

    Batroxobin was recognized for its properties as a coagulant – a substance that encourages blood to clot – in 1936. It has been used in various therapies as a way to remove excess fibrin proteins from the blood to treat thrombosis and as a topical hemostat. It has also been used as a diagnostic tool to determine blood-clotting time in the presence of heparin, an anti-coagulant drug.

    “From a clinical perspective, that’s far and away the most important issue here,” Hartgerink said. “There’s a lot of different things that can trigger blood coagulation, but when you’re on heparin, most of them don’t work, or they work slowly or poorly. That obviously causes problems if you’re bleeding.

    “Heparin blocks the function of thrombin, an enzyme that begins a cascade of reactions that lead to the clotting of blood,” he said. “Batroxobin is also an enzyme with similar function to thrombin, but its function is not blocked by heparin. This is important because surgical bleeding in patients taking heparin can be a serious problem. The use of batroxobin allows us to get around this problem because it can immediately start the clotting process, regardless of whether heparin is there or not.”

    The batroxobin combined with the Rice lab’s hydrogels isn’t taken directly from snakes, Hartgerink said. The substance used for medicine is produced by genetically modified bacteria and then purified, avoiding the risk of other contaminant toxins.

    The Rice researchers combined batroxobin with their synthetic, self-assembling nanofibers, which can be loaded into a syringe and injected at the site of a wound, where they reassemble themselves into a gel.

    Tests showed the new material stopped a wound from bleeding in as little as six seconds, and further prodding of the wound minutes later did not reopen it. The researchers also tested several other options: the hydrogel without batroxobin, the batroxobin without the hydrogel, a current clinical hemostat known as GelFoam and an alternative self-assembling hemostat known as Puramatrix and found that none were as effective, especially in the presence of anti-coagulants.

    The new work builds upon the Rice lab’s extensive development of injectable hydrogel scaffolds that help wounds heal and grow natural tissue. The synthetic scaffolds are built from the peptide sequences to mimic natural processes.

    “To be clear, we did not discover nor do any of the initial investigations of batroxobin,” Hartgerink said. “Its properties have been well-known for many decades. What we did was combine it with the hydrogel we’ve been working on for a long time.

    “We think SB50 has great potential to stop surgical bleeding, particularly in difficult cases in which the patient is taking heparin or other anti-coagulants,” he said. “SB50 takes the powerful clotting ability of this snake venom and makes it far more effective by delivering it in an easily localized hydrogel that prevents possible unwanted systemic effects from using batroxobin alone.”

    SB50 will require FDA approval before clinical use, Hartgerink said. While batroxobin is already approved, the Rice lab’s hydrogel has not yet won approval, a process he expects will take several more years of testing.

    Co-authors of the paper are Rice graduate student Navindee Wickremasinghe and undergraduate Siyu (Kalian) Shi. Kumar is a postdoctoral research fellow in Hartgerink’s group. Hartgerink is a professor of chemistry and of bioengineering.

    The National Institutes of Health and the Welch Foundation supported the research.


    Read the abstract at http://pubs.acs.org/doi/abs/10.1021/acsbiomaterials.5b00356

    See the full article here .

    Please help promote STEM in your local schools.

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    In his 1912 inaugural address, Rice University president Edgar Odell Lovett set forth an ambitious vision for a great research university in Houston, Texas; one dedicated to excellence across the range of human endeavor. With this bold beginning in mind, and with Rice’s centennial approaching, it is time to ask again what we aspire to in a dynamic and shrinking world in which education and the production of knowledge will play an even greater role. What shall our vision be for Rice as we prepare for its second century, and how ought we to advance over the next decade?

    This was the fundamental question posed in the Call to Conversation, a document released to the Rice community in summer 2005. The Call to Conversation asked us to reexamine many aspects of our enterprise, from our fundamental mission and aspirations to the manner in which we define and achieve excellence. It identified the pressures of a constantly changing and increasingly competitive landscape; it asked us to assess honestly Rice’s comparative strengths and weaknesses; and it called on us to define strategic priorities for the future, an effort that will be a focus of the next phase of this process.

  • richardmitnick 5:37 am on October 26, 2015 Permalink | Reply
    Tags: , , Medicine,   

    From ANU: “New gene a key to fighting sepsis” 

    ANU Australian National University Bloc

    Australian National University

    Co-author Linda Fitzgerald works on the multi-pipettor at the Australian Phenomics Centre. Image Stuart Hay, ANU

    Scientists have identified a gene that could potentially open the door for the development of new treatments of the lethal disease sepsis.

    Researchers from The Australian National University (ANU) and the Garvan Institute of Medical Research worked with Genentech, a leading United States biotechnology company, to identify a gene that triggers the inflammatory condition that can lead to the full-body infection sepsis.

    “Isolating the gene so quickly was a triumph for the team,” said Professor Simon Foote, Director of The John Curtin School of Medical Research (JCSMR) at ANU.

    Sepsis is a severe whole-body infection that kills an estimated one million people in the US alone each year. It occurs as a complication to an existing infection, and if not treated quickly can lead to septic shock and multiple organ failure, with death rates as high as 50 per cent.

    Professor Foote acknowledged the vital support of the Australian Government’s National Collaborative Research Infrastructure Strategy in setting up the Australian Phenomics Facility at the JCSMR, where the gene was identified.

    Researchers were aware that sepsis occurs when molecules known as lipopolysaccharides (LPS) on the surface of some bacteria infiltrate cells, triggering an immune response that causes the cells to self-destruct. But exactly how the self-destruct button was pressed remained a mystery.

    Scientists at Genentech showed that Gasdermin-D usually exists in cells in an inactive form. When the LPS molecules enter the cells they trigger an enzyme called caspase-11, a kind of chemical hatchet, to lop the protective chemical cap off Gasdermin-D, which in turn leads the cells to self-destruct.

    The team employed a large-scale forward genetics discovery platform to screen thousands of genes for those involved in the LPS driven self-destruct pathway of cells.

    The team found that the new gene created a protein, Gasdermin-D, that triggers cell death as part of the pathway to sepsis.

    Nobuhiko Kayagaki, PhD, Senior Scientist from Genentech, said the work will help researchers understand and treat other diseases as well as sepsis.

    “The identification of Gasdermin-D can give us a better understanding not only of lethal sepsis, but also of multiple other inflammatory diseases,” he said.

    Professor Chris Goodnow, from ANU and Garvan Institute of Medical Research was a co-author on the research paper, which was published in Nature.

    “This finding is a key that could potentially unlock our ability to shutdown this killer disease before it gets to a life-threatening stage,” Professor Goodnow said.

    See the full article here .

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    ANU is a world-leading university in Australia’s capital city, Canberra. Our location points to our unique history, ties to the Australian Government and special standing as a resource for the Australian people.

    Our focus on research as an asset, and an approach to education, ensures our graduates are in demand the world-over for their abilities to understand, and apply vision and creativity to addressing complex contemporary challenges.

  • richardmitnick 8:08 am on October 20, 2015 Permalink | Reply
    Tags: , , , Medicine, Microsoft   

    From Hopkins: “Johns Hopkins, Microsoft to develop technology to improve patient safety in the ICU” 

    Johns Hopkins
    Johns Hopkins University

    Lisa Broadhead

    Image: istock

    The Johns Hopkins University School of Medicine and Microsoft have announced plans to work together to redesign the way medical devices in an intensive care unit talk to each other.

    The two organizations plan to develop a health IT solution that collects data from different monitoring equipment and identifies key trends aimed at preventing injuries and complications that can result from medical care.

    The idea stems from the Johns Hopkins Armstrong Institute for Patient Safety and Quality’s research on checklists to reduce infections and its pilot program called Project Emerge, which uses technology to restructure a hospital’s workflow in an effort to eliminate the most common causes of preventable harm and promote better patient outcomes. While most efforts to improve safety focus on one harm, Project Emerge seeks to eliminate all harms, including medical complications such as blood clots and pneumonia, as well as emotional harms like a lack of respect and dignity.

    “Today’s intensive care patient room contains anywhere from 50 to 100 pieces of medical equipment developed by different manufacturers that rarely talk to one another,” says Peter Pronovost, senior vice president of patient safety and quality for Johns Hopkins Medicine and director of the Armstrong Institute. “We are excited to collaborate with Microsoft to bring interoperability to these medical devices, to fully realize the benefits of technology and provide better care to our patients and their families. By combining teamwork with technology designed to meet patients’ and clinicians’ needs, we can make care safer, less expensive, and more joyful.”

    Four million patients are admitted to ICUs in the U.S. each year, and between 210,000 and 400,000 patients die annually from a potentially preventable complication, making medical errors the third leading cause of death, behind heart disease and cancer.

    In collaboration with Microsoft, Johns Hopkins plans to revamp Project Emerge to better serve patients in intensive care environments. Johns Hopkins will supply the clinical expertise for the build, while Microsoft will provide advanced technologies, including Azure cloud platform and services, as well as software development expertise. Using Azure, the improved solution will collect and integrate information from several modern devices and provide critical analytics, computing, database, mobility, networking, storage, and Web functions. The final product will allow physicians to see trends in a patient’s care in one centralized location and let them access critical patient information from any hospital-approved, Windows device. Pilot projects are estimated to begin in 2016.

    “Johns Hopkins and Microsoft share a common vision of providing better care to more people,” says Michael Robinson, vice president of U.S. health and life sciences at Microsoft. “Through our joint work, Johns Hopkins and Microsoft will empower health professionals with easy-to-consume, data-driven insights, allowing them to focus more on patients and less on technology and process.”

    This initiative is one of several collaborations between the two organizations designed to foster innovative, health-based technologies. Earlier this year, Microsoft became a sponsor of FastForward, Johns Hopkins’ new business incubator designed to accelerate product development for health IT startup companies. Johns Hopkins also recently joined Microsoft’s Partner Network, which provides enhanced services to the university.

    “Collaborating with Microsoft on multiple fronts will provide mutually beneficial opportunities that can change the face of the health information technology landscape,” says Christy Wyskiel, senior advisor to the president of The Johns Hopkins University and head of Johns Hopkins Technology Ventures. “I look forward to harnessing these opportunities and seeing many positive outcomes from our relationship.”

    The initial build of Project Emerge was funded by the Gordon and Betty Moore Foundation. The Armstrong Institute, Johns Hopkins University Applied Physics Laboratory, and the University of California, San Francisco, collaborated on the project to develop and test the initial prototype.

    See the full article here .

    Please help promote STEM in your local schools.
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    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.

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