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  • richardmitnick 9:39 am on September 17, 2014 Permalink | Reply
    Tags: , , Medicine, Stem Cell Research   

    From New Scientist: “Stem cells used in landmark therapy for failing sight” 

    NewScientist

    New Scientist

    17 September 2014
    Andy Coghlan

    A woman in Japan has received the first medical treatment based on induced pluripotent stem cells, eight years after they were discovered.

    The iPS cells were made by reprogramming skin cells from the woman’s arm, then transformed into specialised eye cells to treat age-related macular degeneration (AMD) ´ a condition that affects millions of elderly people worldwide, and often results in blindness. Last week, the woman, who is in her 70s, had a patch of the cells measuring 1.3 by 3 millimetres grafted into her eye in a two-hour operation.

    eye
    Grafts derived from stem cells could keep the retina in good working order (Image: Science Source/Science Photo Library)

    She is the first of six people lined up for the landmark treatment, developed by Masayo Takahashi and her colleagues at the RIKEN Center for Developmental Biology in Kobe, Japan. In a pilot study to test the safety of putting iPS-derived cells into humans, the six are all receiving a graft of new retinal pigment epithelial (RPE) cells, which serve to maintain the eye’s light-sensing cells.

    No embryos needed

    Since iPS cells can be made from adult tissue samples, the technique does not require the destruction of embryos, unlike stem-cell-based AMD treatments that are also being worked on – one such treatment is being trialled in the US and UK.

    “It’s an exciting development, and we await the outcome over the next year to see how well these cells integrate, and if there are any potential adverse reactions,” says Mike Cheetham of the Institute of Ophthalmology at University College London, one site which is also researching a human embryonic stem-cell treatment for AMD. “If it goes well, it could be the start of a new era in personalised medicine,” he says.

    Shinya Yamanaka and his colleagues at Kyoto University in Japan discovered iPS cells in 2006. In 2012, Yamanaka was awarded the Nobel prize for the work.

    See the full article here.

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  • richardmitnick 2:12 pm on September 15, 2014 Permalink | Reply
    Tags: , , Harvard University, Medicine   

    From NOVA: “‘Biospleen Device’ Uses Magnetic Nanoparticles to Filter Pathogens from Blood” 

    PBS NOVA

    NOVA

    Mon, 15 Sep 2014
    Tim De Chant

    When a patient succumbs to an infection, it’s not the mere presence of the pathogen that kills them, but rather the sheer quantity of it. With many deadly diseases, the immune system simply can’t keep up. So bioengineers figured that outsourcing some of those duties could help keep patients alive.

    A team of bioengineers led by Donald Ingber at Harvard’s Wyss Institute devised a device to filter pathogens from a patient’s blood. Inspired by the spleen, an organ which filters antibody-coated pathogens from the bloodstream, the “biospleen” works by first injecting specially treated, magnetic nanoparticles into the blood flowing through it. The nanoparticles have a protein attached to their surfaces which adheres to bacteria, viruses, and fungi; the protein-coated nanoparticles work like antibodies, which glom onto foreign objects. The biospleen then uses a magnet to pull out the nanoparticles and the pathogens they’re attached to.

    bio
    The filtering section of the biospleen

    The biospleen is similar in concept to dialysis, which mimics the function of the kidneys, but works on pathogens instead of typical bodily waste.

    Sara Reardon, reporting for Nature News, has more details:

    To test the device, Ingber and his team infected rats with either E. coli or Staphylococcus aureus and filtered blood from some of the animals through the biospleen. Five hours after infection, 89% of the rats whose blood had been filtered were still alive, compared with only 14% of those that were infected but not treated. The researchers found that the device had removed more than 90% of the bacteria from the rats’ blood. The rats whose blood had been filtered also had less inflammation in their lungs and other organs, suggesting they would be less prone to sepsis.

    Ingber and his team also tested the device using human volumes of blood, and they found that it took about five hours to filter most pathogens from five liters of blood.

    If the device makes it into trials, which could happen in just a few years, it could give doctors the upper hand in a number of intractable infections, including HIV and Ebola. The biospleen could reduce the pathogen load in a patient’s blood, leaving the drugs that normally treat the infection to clear the virus or bacteria from the patient’s organs. In acute infections, like Ebola, it would also buy doctors valuable time in their efforts to eliminate the virus before the patient succumbs.

    See the full article here.

    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.

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  • richardmitnick 10:10 am on September 14, 2014 Permalink | Reply
    Tags: , , , Medicine, New Technology,   

    From Rutgers- “Novel Local Morphologic Scale: Applications in Disease Diagnosis and Prognosis” 

    Rutgers University
    Rutgers University

    Rutgers Technology

    Invention Summary

    Timely and accurate diagnosis of disease pathologies is critical to providing effective treatment to patients. Rutgers scientists have developed a novel local morphologic scale (LMS) to rapidly and automatically select, quantify and classify tissue/specimen topologies using parallelized computations. This unique tool has the ability to define features for every special image location and generate subsequent scene segmentation and classification for each location. Further this technology is free from shape constraints and generates output based on local structure attributes of complex histological images. This innovation has been successfully utilized in discriminating tumor versus stromal regions by classifying oncogenic tumor infiltrating lymphocytes (biomarker) in ovarian cancer tissue microarrays. Additionally, this technology has been applied across 3 other domains (prostate, breast) under two different stains illustrating its robustness to domain selection. This technology can be immensely useful to identify regions of interest, model heterogeneity of the underlying topology and generate digital signatures. It can also be used to train supervised classifiers to identify similar structural signatures in an image and therefore reduce or eliminate and observer variability.

    Market Application

    Disease Diagnosis, Digital Pathology, Histopathology, Computer Aided Diagnosis (CAD), Tissue Classification, Disease Monitoring and Prognosis, Lymphocyte Infiltration, Cancer.

    Advantages

    Signatures derived from cancerous versus non-cancerous tissues differ greatly. This tool can be highly instrumental in classifying cancerous versus non-cancerous tissue, can reliably and accurately account for cell shape and phenotypes, and provide accurate tissue classification, enabling pathologists to visually discern the two regions.

    Intellectual Property & Development Status
    Patent pending.

    Select Publication
    Janowczyk, A, Chandran S, Feldman MD, Madabhushi A. (2011). Local morphologic scale: Application to segmenting tumor infiltrating lymphocytes in ovarian cancer TMAs. SPIE http://lcib.rutgers.edu/publications/ Andrew/SPIE2011.pdf

    See the full articled here.

    Rutgers, The State University of New Jersey, is a leading national research university and the state’s preeminent, comprehensive public institution of higher education. Rutgers is dedicated to teaching that meets the highest standards of excellence; to conducting research that breaks new ground; and to providing services, solutions, and clinical care that help individuals and the local, national, and global communities where they live.

    Founded in 1766, Rutgers teaches across the full educational spectrum: preschool to precollege; undergraduate to graduate; postdoctoral fellowships to residencies; and continuing education for professional and personal advancement.

    Rutgers Seal

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  • richardmitnick 9:43 am on September 14, 2014 Permalink | Reply
    Tags: , , , , Medicine,   

    From M.I.T Tech Review: “Gene-Silencing Drugs Finally Show Promise” 

    MIT Technology Review
    M.I.T Technology Review

    September 14, 2014
    Kevin Bullis

    After more than a decade of disappointment, a startup leads the development of a powerful new class of drugs based on a Nobel-winning idea.

    The disease starts with a feeling of increased clumsiness. Spilling a cup of coffee. Stumbling on the stairs. Having accidents that are easy to dismiss—everyone trips now and then.

    But it inevitably gets worse. Known as familial amyloid polyneuropathy, or FAP, it can go misdiagnosed for years as patients lose the ability to walk or perform delicate tasks with their hands. Most patients die within 10 to 15 years of the first symptoms.

    There is no cure. The disease is caused by malformed proteins produced in the liver, so one treatment is a liver transplant. But few patients can get one—and it only slows the disease down.

    Now, after years of false starts and disappointment, it looks like an audacious idea for helping these patients finally could work.

    In 1998, researchers at the Carnegie Institution and the University of Massachusetts made a surprising discovery about how cells regulate which proteins they produce. They found that certain kinds of RNA—which is what DNA makes to create proteins—can turn off specific genes. The finding, called RNA interference (RNAi), was exciting because it suggested a way to shut down the production of any protein in the body, including those connected with diseases that couldn’t be touched with ordinary drugs. It was so promising that its discoverers won the Nobel Prize just eight years later.

    Inspired by the discovery, another group of researchers—including the former thesis supervisor of one of the Nobel laureates—founded Alnylam in Cambridge, Massachusetts, in 2002. Their goal: fight diseases like FAP by using RNAi to eliminate bad proteins (see “The Prize of RNAi” and “Prescription RNA”). Never mind that no one knew how to make a drug that could trigger RNAi. In fact, that challenge would bedevil the researchers for the better part of a decade. Along the way, the company lost the support of major drug companies that had signed on in a first wave of enthusiasm. At one point the idea of RNAi therapy was on the verge of being discredited.

    But now Alnylam is testing a drug to treat FAP in advanced human trials. It’s the last hurdle before the company will seek regulatory approval to put the drug on the market. Although it’s too early to tell how well the drug will alleviate symptoms, it’s doing what the researchers hoped it would: it can decrease the production of the protein that causes FAP by more than 80 percent.

    This could be just the beginning for RNAi. Alnylam has more than 11 drugs, including ones for hemophilia, hepatitis B, and even high cholesterol, in its development pipeline, and has three in human trials —progress that led the pharmaceutical company Sanofi to make a $700 million investment in the company last winter. Last month, the pharmaceutical giant Roche, an early Alnylam supporter that had given up on RNAi, reversed its opinion of the technology as well, announcing a $450 million deal to acquire the RNAi startup Santaris. All told, there are about 15 RNAi-based drugs in clinical trials from several research groups and companies.

    “The world went from believing RNAi would change everything to thinking it wouldn’t work, to now thinking it will,” says Robert Langer, a professor at MIT, and one of Alnylam’s advisors.

    Delivering Drugs

    Alnylam started with high hopes. Its founders, among them the Nobel laureate and MIT biologist Philip Sharp, had solved one of the biggest challenges facing the idea of RNAi therapies. When RNAi was discovered, the process was triggered by introducing a type of RNA, called double stranded RNA, into cells. This worked well in worms and fruit flies. But the immune system in mammals reacted violently to the RNA, causing cells to die and making the approach useless except as a research tool. The Alnylam founders figured out that shorter strands, called siRNA, could slip into mammalian cells without triggering an immune reaction, suggesting a way around this problem.

    Yet another huge problem remained. RNA interference depends upon delivering RNA to cells, tricking the cells into allowing it through the protective cell membrane, and then getting the cells to incorporate it into molecular machinery that regulates proteins. Scientists could do this in petri dishes but not in animals.

    Alnylam looked everywhere for solutions, scouring the scientific literature, collaborating with other companies, considering novel approaches of its own. It focused on two options. One was encasing RNA in bubbles of fat-like nanoparticles of lipids. They are made with the same materials that make up cell membranes—the thought was that the cell would respond well to the familiar substance. The other approach was attaching a molecule to the RNA that cells like to ingest, tricking the cell into eating it.

    And both approaches worked, sort of. Researchers were able to block protein production in lab animals. But getting the delivery system right wasn’t easy. The early mechanisms were too toxic at the doses required to be used as drugs.

    As a result, delivering RNA through the bloodstream like a conventional drug seemed a far-off prospect. The company tried a shortcut of injecting chemically modified RNA directly into diseased tissue —for example, into the retina to treat eye diseases. That approach even got to clinical trials. But it was shelved because it didn’t perform as well as up-and-coming drugs from other companies.

    By 2010, some of the major drug companies that were working with and investing in Alnylam lost patience. Novartis decided not to extend a partnership with Alnylam; Roche gave up on RNAi altogether. Alnylam laid off about a quarter of its workers, and by mid-2011, its stock price had plunged by 80 percent from its peak.

    But Alnylam and partner companies, notably the Canadian startup Tekmira, were making steady progress in the lab. Researchers identified one part of the lipid nanoparticles that was keeping them from delivering its cargo of RNA to the right part of a cell. That was “the real eureka moment,” says Rachel Meyers, Alnylam’s vice president of research. Better nanoparticles improved the potency of a drug a hundredfold and its safety by about five times, clearing the way for clinical trials for FAP—a crucial event that kept the company alive.

    Even with that progress, Alnylam needed more. The nanoparticle delivery mechanism is costly to make and requires frequent visits to the hospital for hour-long IV infusions—something patients desperate to stay alive will put up with, but likely not millions of people with high cholesterol.

    So Alnylam turned to its second delivery approach—attaching molecules to RNA to trick cells into ingesting it. Researchers found just the right inducement—attaching a type of sugar molecule. This approach allows for the drug to be administered with a simple injection that patients could give themselves at home.

    In addition to being easier to administer, the new sugar-based drugs are potentially cheaper to make. The combination of low cost and ease-of-use is allowing Alnylam to go after more common diseases—not just the rare ones that patients will go to great lengths to treat. “Because we’ve made incredible improvements in the delivery strategy,” Meyers says, “we can now go after big diseases where we can treat millions of patients potentially.”

    The Next Frontier

    In a sixth-floor lab on the MIT campus, postdoctoral researcher James Dahlman takes down boxes from a high shelf. They contain hundreds of vials, each containing a unique type of nanoparticle that Dahlman synthesized painstakingly, one at a time. “It turns out we have a robot in the lab that can do that,” he says. “But I didn’t know about it at the time.”

    Dahlman doesn’t work for Alnylam; he had been searching for the next great delivery mechanism, one that could greatly expand the diseases that can be treated by RNAi. Some of the materials look like clear liquids. Some are waxy, some like salt crystals. He points to a gap in the rows of vials, where a vial is conspicuously missing. “That’s the one that worked. That’s the miracle material,” he says.

    For all of their benefits, the drug delivery mechanisms Alnylam uses have one flaw—they’re effective only for delivering drugs to liver cells. For a number of reasons, the liver is a relatively easy target—that’s where all kinds of nanoparticles tend to end up. Alnylam sees the potential for billions of dollars in revenue from liver-related diseases. Yet most diseases involve other tissues in the body.

    Dahlman and his colleagues at MIT are some of the leaders in the next generation of RNAi delivery—targeting delivery to places throughout the body. Last month, in two separate articles, they published the results of studies showing that Dahlman’s new nanoparticles are a powerful way to deliver RNAi to blood vessel cells, which are associated with a wide variety of diseases. The studies showed that the method could be used to reduce tumor growth in lung cancer, for example.

    Treating cancer is one area where RNAi’s particular advantages are expected to shine. Conventional chemotherapy affects more than just the target cancer cells—it also hurts healthy tissue, which is why it makes people feel miserable. But RNAi can be extremely precise, potentially shutting down only proteins found in cancer cells. And Dahlman’s latest delivery system makes it possible to simultaneously target up to 10 proteins at once, which could make cancer treatments far more effective. Lab work like this is far from fruition, but if it maintains its momentum, the drugs currently in clinical trials could represent just a small portion of the benefits of the discovery of RNAi.

    See the full article here.

    The mission of MIT Technology Review is to equip its audiences with the intelligence to understand a world shaped by technology.

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  • richardmitnick 3:43 pm on September 12, 2014 Permalink | Reply
    Tags: , , , Medicine,   

    From DESY: “Researchers X-Ray Living Cancer Cells” 

    DESY
    DESY

    27.02.2014

    Nanodiffraction opens up new insights into the physics of life

    Göttingen-based scientists working at DESY’s PETRA III research light source have carried out the first studies of living biological cells using high-energy X-rays. The new method shows clear differences in the internal cellular structure between living and dead, chemically fixed cells that are often analysed. “The new method for the first time enables us to investigate the internal structures of living cells in their natural environment using hard X-rays,” emphasises the leader of the working group, Prof. Sarah Köster from the Institute for X-Ray Physics of the University of Göttingen. The researchers present their work in the scientific journal Physical Review Letters.
    Zoom (17 KB)

    c ells
    X-ray scan of chemically fixed cells. Each pixel represents a full diffraction image. The colours indicate how strong the X-rays are scattered at each individual point. Credit: Britta Weinhausen/University of Göttingen

    Thanks to analytical methods with ever-higher resolution, scientists today can study biological cells at the level of individual molecules. The cells are frequently chemically fixed before they are studied with the help of optical, X-ray or electron microscopes. The process of chemical fixation involves immersing the cells in a type of chemical preservative which fixes all of the cell’s organelles and even the proteins in place. “Minor changes to the internal structure of the cells are unavoidable in this process,” emphasises Köster. “In our studies, we were able to show these changes in direct comparison for the first time.”

    The team used cancer cells from the adrenal cortex for their analyses. They grew the cells on a silicon nitrite substrate, which is almost transparent to X-rays. In order to keep the cells alive in the experimental chamber during the experiment, they were supplied with nutrients, and their metabolic products were pumped away via fine channels just 0.5 millimetres in diameter. “The biological cells are thus located in a sample environment which very closely resembles their natural environment,” explains Dr. Britta Weinhausen from Köster’s group, the paper’s first author.

    The experiments were carried out at the Nanofocus Setup (GINIX) of PETRA III’s experimental station P10. The scientists used the brilliant X-ray beam from PETRA III to scan the cells in order to obtain information about their internal nanostructure. “Each frame was exposed for just 0.05 seconds, in order to avoid damaging the living cells too quickly”, explains co-author Dr. Michael Sprung from DESY. “Even nanometre-scale structures can be measured with the GINIX assembly, thanks to the combination of PETRA III’s high brilliance and the GINIX setup which is matched to the source.”

    The researchers studied living and chemically fixed cells using this so-called nanodiffraction technique and compared the cells’ internal structures on the basis of the X-ray diffraction images. The results showed that the chemical fixation produces noticeable differences in the cellular structure on a scale of 30 to 50 nanometres (millionths of a millimetre).

    “Thanks to the ever-greater resolution of the various investigative techniques, it is increasingly important to know whether the internal structure of the sample changes during sample preparation,” explains Köster. In future, the new technique will make it possible to study unchanged living cells at high resolution. Although other methods have an even higher resolution than X-ray scattering, they require a chemical fixation or complex and invasive preparation of the cells. Lower-energy, so-called soft X-rays have already been used for studies of living cells. However, the study of structures with sizes as small as 12 nanometres first becomes possible through the analysis of diffraction images produced using hard X-rays.

    See the full article here.

    desi

    DESY is one of the world’s leading accelerator centres. Researchers use the large-scale facilities at DESY to explore the microcosm in all its variety – from the interactions of tiny elementary particles and the behaviour of new types of nanomaterials to biomolecular processes that are essential to life. The accelerators and detectors that DESY develops and builds are unique research tools. The facilities generate the world’s most intense X-ray light, accelerate particles to record energies and open completely new windows onto the universe. 
That makes DESY not only a magnet for more than 3000 guest researchers from over 40 countries every year, but also a coveted partner for national and international cooperations. Committed young researchers find an exciting interdisciplinary setting at DESY. The research centre offers specialized training for a large number of professions. DESY cooperates with industry and business to promote new technologies that will benefit society and encourage innovations. This also benefits the metropolitan regions of the two DESY locations, Hamburg and Zeuthen near Berlin.

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  • richardmitnick 2:33 pm on September 12, 2014 Permalink | Reply
    Tags: , , Medicine, ,   

    From physicsworld: “Synchrotron X-rays track fluids in the lungs” 

    physicsworld
    physicsworld.com

    Sep 12, 2014
    Ian Randall

    A new method of soft-tissue imaging could allow doctors to monitor respiratory treatments of cystic-fibrosis patients, reports an international research team. The technique – which measures the refraction of a grid pattern of X-rays passing through the lungs – has been successfully demonstrated in live mice, and could eventually find application in visualizing other soft tissues, such as the brain and heart.

    synchro
    Synchrotron source: phase-contrast imaging in the lab

    Cystic fibrosis is a life-threatening genetic disorder that affects the exocrine glands, resulting in unusually thick secretions of mucus. In lungs, mucus is supposed to keep the airways moist, along with forming a conveyor belt, moved by beating cilia, which carries away foreign particles and pathogens. In cystic-fibrosis patients, however, the thicker mucus flows less easily – resulting in a build-up that can cause inflammation, breathing difficulties and increased susceptibility to bacterial infection.

    Respiratory therapies for cystic-fibrosis patients typically focus on increasing hydration of the airways to improve mucus flow. Tracking the progress of these treatments, however, is challenging. “At the moment, we typically need to wait for a cystic-fibrosis treatment to have an effect on lung health, measured by either a lung CT scan or breath measurement, to see how effective it is,” explains lead researcher Kaye Morgan from Monash University in Australia. With successful medications often taking months to have a measurable impact, progress in developing new treatments is correspondingly slow.

    Fast yet sensitive

    The challenge lies in imaging the surface layers of liquid in the airways. These are usually only a few tens of microns across, bear a close resemblance to the underlying tissue and – given the passage of air in and out of lungs – constantly move around. Consequently, any technique for imaging this interface needs to be high-resolution, as well as sufficiently fast and sensitive.

    mouse
    Single-grid-based phase-contrast X-ray imaging reveals a liquid surface layer in the lungs of a live mouse
    Sharper image: X-rays reveal a liquid surface layer

    Morgan and colleagues have developed an imaging method that they call single-grid-based phase-contrast X-ray imaging. Unlike conventional radiography, which measures the absorption of X-rays, the new approach measures the refraction of a grid pattern of radiation as it passes through the soft tissues.

    “A good analogy is the patterns we see on the bottom of swimming pools,” explains Morgan. At the detector, the X-ray grid will appear distorted in accordance with the properties of the tissues that the rays have passed through – much in the same way that tiles in a pool appear distorted when seen through water. “By tracking the distortions in the grid pattern, we can reconstruct the airway structures.”

    Anaesthetized mice

    To test their method, the researchers imaged the airways of eight anaesthetized mice. Using a nebulizer, each mouse was treated first with a saline control solution, and then with a treatment designed to block the dehydrating effect of the cells lining the airway. X-rays from a synchrotron travelled through a 25.4 µm grid to create the desired pattern; this produced images at the detector with 0.18 µm-sized pixels. Images were recorded at three-minute intervals for 15 minutes after each treatment.

    By tracking the distortions in the grid pattern, we can reconstruct the airway structures
    Kaye Morgan, Monash University

    The method successfully imaged the airway, surface liquids and underlying tissues. A noticeable increase in the surface hydration depth was observed after treatment in comparison with the control. “The new imaging method allows us, for the first time, to non-invasively see how the treatment is working, ‘live’ on the airway surface,” Morgan says.

    “This is a novel and interesting biomedical application,” says Mark Anastasio, a biomedical engineer from Washington University in St Louis. With existing solutions unable to reveal such subtle soft-tissue interfaces, he adds, this result “motivates the further development of X-ray phase-contrast imaging technologies”.
    Practical issues

    Ke Li, a medical physicist from the University of Wisconsin-Madison, points out that making measurements on live mice “is a huge step along the course of applying phase-contrast X-ray projection imaging to medical imaging”. However, Li questions the practicality of using a synchrotron X-ray source in a clinical environment, especially given the high radiation dose necessary for such an ultra-fine pixel size.

    Some of these concerns could soon be addressed, with Morgan and colleagues now exploring how their work might translate into a clinical setting. At the same time, the team is investigating other possible medical applications, looking both at lungs and other soft tissues, such as the brain and heart.

    See the full article here.

    PhysicsWorld is a publication of the Institute of Physics. The Institute of Physics is a leading scientific society. We are a charitable organisation with a worldwide membership of more than 50,000, working together to advance physics education, research and application.

    We engage with policymakers and the general public to develop awareness and understanding of the value of physics and, through IOP Publishing, we are world leaders in professional scientific communications.
    IOP Institute of Physics

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  • richardmitnick 7:45 am on September 9, 2014 Permalink | Reply
    Tags: , , , Medicine,   

    From PBS NOVA: “Why There’s No HIV Cure Yet” 

    PBS NOVA

    NOVA

    Wed, 27 Aug 2014
    Alison Hill

    Over the past two years, the phrase “HIV cure” has flashed repeatedly across newspaper headlines. In March 2013, doctors from Mississippi reported that the disease had vanished in a toddler who was infected at birth. Four months later, researchers in Boston reported a similar finding in two previously HIV-positive men. All three were no longer required to take any drug treatments. The media heralded the breakthrough, and there was anxious optimism among HIV researchers. Millions of dollars of grant funds were earmarked to bring this work to more patients.

    But in December 2013, the optimism evaporated. HIV had returned in both of the Boston men. Then, just this summer, researchers announced the same grim results for the child from Mississippi. The inevitable questions mounted from the baffled public. Will there ever be a cure for this disease? As a scientist researching HIV/AIDS, I can tell you there’s no straightforward answer. HIV is a notoriously tricky virus, one that’s eluded promising treatments before. But perhaps just as problematic is the word “cure” itself.

    Science has its fair share of trigger words. Biologists prickle at the words “vegetable” and “fruit”—culinary terms which are used without a botanical basis—chemists wrinkle their noses at “chemical free,” and physicists dislike calling “centrifugal” a force—it’s not; it only feels like one. If you ask an HIV researcher about a cure for the disease, you’ll almost certainly be chastised. What makes “cure” such a heated word?

    cells
    HIV hijacks the body’s immune system by attacking T cells.

    It all started with a promise. In the early 1980s, doctors and public health officials noticed large clusters of previously healthy people whose immune systems were completely failing. The new condition became known as AIDS, for “acquired immunodeficiency syndrome.” A few years later, in 1984, researchers discovered the cause—the human immunodeficiency virus, now known commonly as HIV. On the day this breakthrough was announced, health officials assured the public that a vaccine to protect against the dreaded infection was only two years away. Yet here we are, 30 years later, and there’s still no vaccine. This turned out to be the first of many overzealous predictions about controlling the HIV epidemic or curing infected patients.

    The progression from HIV infection to AIDS and eventual death occurs in over 99% of untreated cases—making it more deadly than Ebola or the plague. Despite being identified only a few decades ago, AIDS has already killed 25 million people and currently infects another 35 million, and the World Health Organization lists it as the sixth leading cause of death worldwide.

    HIV disrupts the body’s natural disease-fighting mechanisms, which makes it particularly deadly and complicates efforts to develop a vaccine against it. Like all viruses, HIV gets inside individual cells in the body and highjacks their machinery to make thousands of copies of itself. HIV replication is especially hard for the body to control because the white blood cells it infects, and eventually kills, are a critical part of the immune system. Additionally, when HIV copies its genes, it does so sloppily. This causes it to quickly mutate into many different strains. As a result, the virus easily outwits the body’s immune defenses, eventually throwing the immune system into disarray. That gives other obscure or otherwise innocuous infections a chance to flourish in the body—a defining feature of AIDS.
    Early Hope

    In 1987, the FDA approved AZT as the first drug to treat HIV. With only two years between when the drug was identified in the lab and when it was available for doctors to prescribe, it was—and remains—the fastest approval process in the history of the FDA. AZT was widely heralded as a breakthrough. But as the movie The Dallas Buyer’s Club poignantly retells, AZT was not the miracle drug many hoped. Early prescriptions often elicited toxic side-effects and only offered a temporary benefit, as the virus quickly mutated to become resistant to the treatment. (Today, the toxicity problems have been significantly reduced, thanks to lower doses.) AZT remains a shining example of scientific bravura and is still an important tool to slow the infection, but it is far from the cure the world had hoped for.

    In three decades, over 25 highly-potent drugs have been developed and FDA-approved to treat HIV.

    Then, in the mid-1990s, some mathematicians began probing the data. Together with HIV scientists, they suggested that by taking three drugs together, we could avoid the problem of drug resistance. The chance that the virus would have enough mutations to allow it to avoid all drugs at once, they calculated, would simply be too low to worry about. When the first clinical trials of these “drug cocktails” began, both mathematical and laboratory researchers watched the levels of virus drop steadily in patients until they were undetectable. They extrapolated this decline downwards and calculated that, after two to three years of treatment, all traces of the virus should be gone from a patient’s body. When that happened, scientists believed, drugs could be withdrawn, and finally, a cure achieved. But when the time came for the first patients to stop their drugs, the virus again seemed to outwit modern medicine. Within a few weeks of the last pill, virus levels in patients’ blood sprang up to pre-treatment levels—and stayed there.

    In the three decades since, over 25 more highly-potent drugs have been developed and FDA-approved to treat HIV. When two to five of them are combined into a drug cocktail, the mixture can shut down the virus’s replication, prevent the onset of AIDS, and return life expectancy to a normal level. However, patients must continue taking these treatments for their entire lives. Though better than the alternative, drug regimens are still inconvenient and expensive, especially for patients living in the developing world.

    Given modern medicine’s success in curing other diseases, what makes HIV different? By definition, an infection is cured if treatment can be stopped without the risk of it resurfacing. When you take a week-long course of antibiotics for strep throat, for example, you can rest assured that the infection is on track to be cleared out of your body. But not with HIV.

    A Bad Memory

    The secret to why HIV is so hard to cure lies in a quirk of the type of cell it infects. Our immune system is designed to store information about infections we have had in the past; this property is called “immunologic memory.” That’s why you’re unlikely to be infected with chickenpox a second time or catch a disease you were vaccinated against. When an infection grows in the body, the white blood cells that are best able to fight it multiply repeatedly, perfecting their infection-fighting properties with each new generation. After the infection is cleared, most of these cells will die off, since they are no longer needed. However, to speed the counter-attack if the same infection returns, some white blood cells will transition to a hibernation state. They don’t do much in this state but can live for an extremely long time, thereby storing the “memory” of past infections. If provoked by a recurrence, these dormant cells will reactivate quickly.

    This near-immortal, sleep-like state allows HIV to persist in white blood cells in a patient’s body for decades. White blood cells infected with HIV will occasionally transition to the dormant state before the virus kills them. In the process, the virus also goes temporarily inactive. By the time drugs are started, a typical infected person contains millions of these cells with this “latent” HIV in them. Drug cocktails can prevent the virus from replicating, but they do nothing to the latent virus. Every day, some of the dormant white blood cells wake up. If drug treatment is halted, the latent virus particles can restart the infection.
    Latent HIV’s near-immortal, sleep-like state allows it to persist in white blood cells in a patient’s body for decades.

    HIV researchers call this huge pool of latent virus the “barrier to a cure.” Everyone’s looking for ways to get rid of it. It’s a daunting task, because although a million HIV-infected cells may seem like a lot, there are around a million times that many dormant white blood cells in the whole body. Finding the ones that contain HIV is a true needle-in-a-haystack problem. All that remains of a latent virus is its DNA, which is extremely tiny compared to the entire human genome inside every cell (about 0.001% of the size).

    Defining a Cure

    Around a decade ago, scientists began to talk amongst themselves about what a hypothetical cure could look like. They settled on two approaches. The first would involve purging the body of latent virus so that if drugs were stopped, there would be nothing left to restart the infection. This was often called a “sterilizing cure.” It would have to be done in a more targeted and less toxic way than previous attempts of the late 1990s, which, because they attempted to “wake up” all of the body’s dormant white blood cells, pushed the immune system into a self-destructive overdrive. The second approach would instead equip the body with the ability to control the virus on its own. In this case, even if treatment was stopped and latent virus reemerged, it would be unable to produce a self-sustaining, high-level infection. This approach was referred to as a “functional cure.”

    The functional cure approach acknowledged that latency alone was not the barrier to a cure for HIV. There are other common viruses that have a long-lived latent state, such as the Epstein-Barr virus that causes infectious mononucleosis (“mono”), but they rarely cause full-blown disease when reactivated. HIV is, of course, different because the immune system in most people is unable to control the infection.

    The first hint that a cure for HIV might be more than a pipe-dream came in 2008 in a fortuitous human experiment later known as the “Berlin patient.” The Berlin patient was an HIV-positive man who had also developed leukemia, a blood cancer to which HIV patients are susceptible. His cancer was advanced, so in a last-ditch effort, doctors completely cleared his bone marrow of all cells, cancerous and healthy. They then transplanted new bone marrow cells from a donor.

    Fortunately for the Berlin patient, doctors were able to find a compatible bone marrow donor who carried a unique HIV-resistance mutation in a gene known as CCR5. They completed the transplant with these cells and waited.

    For the last five years, the Berlin patient has remained off treatment without any sign of infection. Doctors still cannot detect any HIV in his body. While the Berlin patient may be cured, this approach cannot be used for most HIV-infected patients. Bone marrow transplants are extremely risky and expensive, and they would never be conducted in someone who wasn’t terminally ill—especially since current anti-HIV drugs are so good at keeping the infection in check.

    Still, the Berlin patient was an important proof-of-principle case. Most of the latent virus was likely cleared out during the transplant, and even if the virus remained, most strains couldn’t replicate efficiently given the new cells with the CCR5 mutation. The Berlin patient case provides evidence that at least one of the two cure methods (sterilizing or functional), or perhaps a combination of them, is effective.

    Researchers have continued to try to find more practical ways to rid patients of the latent virus in safe and targeted ways. In the past five years, they have identified multiple anti-latency drug candidates in the lab. Many have already begun clinical trials. Each time, people grow optimistic that a cure will be found. But so far, the results have been disappointing. None of the drugs have been able to significantly lower levels of latent virus.

    In the meantime, doctors in Boston have attempted to tease out which of the two cure methods was at work in the Berlin patient. They conducted bone marrow transplants on two HIV-infected men with cancer—but this time, since HIV-resistant donor cells were not available, they just used typical cells. Both patients continued their drug cocktails during and after the transplant in the hopes that the new cells would remain HIV-free. After the transplants, no HIV was detectable, but the real test came when these patients volunteered to stop their drug regimens. When they remained HIV-free a few months later, the results were presented at the International AIDS Society meeting in July 2013. News outlets around the world declared that two more individuals had been cured of HIV.

    Latent virus had likely escaped the detection methods available.

    It quickly became clear that everyone had spoken too soon. Six months later, researchers reported that the virus had suddenly and rapidly returned in both individuals. Latent virus had likely escaped the detection methods available—which are not sensitive enough—and persisted at low, but significant levels. Disappointment was widespread. The findings showed that even very small amounts of latent virus could restart an infection. It also meant meant that the anti-latency drugs in development would need to be extremely potent to give any hope of a cure.

    But there was one more hope—the “Mississippi baby.” A baby was born to an HIV-infected mother who had not received any routine prenatal testing or treatment. Tests revealed high levels of HIV in the baby’s blood, so doctors immediately started the infant on a drug cocktail, to be continued for life.

    The mother and child soon lost touch with their health care providers. When they were relocated a few years later, doctors learned that the mother had stopped giving drugs to the child several months prior. The doctors administered all possible tests to look for signs of the virus, both latent and active, but they didn’t find any evidence. They chose not to re-administer drugs, and a year later, when the virus was still nowhere to be found, they presented the findings to the public. It was once again heralded as a cure.

    Again, it was not to be. Just last month, the child’s doctors announced that the virus had sprung back unexpectedly. It seemed that even starting drugs as soon as infection was detected in the newborn could not prevent the infection from returning over two years later.
    Hope Remains

    Despite our grim track record with the disease, HIV is probably not incurable. Although we don’t have a cure yet, we’ve learned many lessons along the way. Most importantly, we should be extremely careful about using the word “cure,” because for now, we’ll never know if a person is cured until they’re not cured.

    Clearing out latent virus may still be a feasible approach to a cure, but the purge will have to be extremely thorough. We need drugs that can carefully reactivate or remove latent HIV, leaving minimal surviving virus while avoiding the problems that befell earlier tests that reactivated the entire immune system. Scientists have proposed multiple, cutting-edge techniques to engineer “smart” drugs for this purpose, but we don’t yet know how to deliver this type of treatment safely or effectively.

    As a result, most investigations focus on traditional types of drugs. Researchers have developed ways to rapidly scan huge repositories of existing medicines for their ability to target latent HIV. These methods have already identified compounds that were previously used to treat alcoholism, cancer, and epilepsy, and researchers are repurposing them to be tested in HIV-infected patients.
    The less latent virus that remains, the less chance there is that the virus will win the game of chance.

    Mathematicians are also helping HIV researchers evaluate new treatments. My colleagues and I use math to take data collected from just a few individuals and fill in the gaps. One question we’re focusing on is exactly how much latent virus must be removed to cure a patient, or at least to let them stop their drug cocktails for a few years. Each cell harboring latent virus is a potential spark that could restart the infection. But we don’t know when the virus will reactivate. Even once a single latent virus awakens, there are still many barriers it must overcome to restart a full-blown infection. The less latent virus that remains, the less chance there is that the virus will win this game of chance. Math allows us to work out these odds very precisely.

    Our calculations show that “apparent cures”—where patients with latent virus levels low enough to escape detection for months or years without treatment—are not a medical anomaly. In fact, math tells us that they are an expected result of these chance dynamics. It can also help researchers determine how good an anti-latency drug should be before it’s worth testing in a clinical trial.

    Many researchers are working to augment the body’s ability to control the infection, providing a functional cure rather than a sterilizing one. Studies are underway to render anyone’s immune cells resistant to HIV, mimicking the CCR5 mutation that gives some people natural resistance. Vaccines that could be given after infection, to boost the immune response or protect the body from the virus’s ill effects, are also in development.

    In the meantime, treating all HIV-infected individuals—which has the added benefit of preventing new transmissions—remains the best way to control the epidemic and reduce mortality. But the promise of “universal treatment” has also not materialized. Currently, even in the U.S., only 25% of HIV-positive people have their viral levels adequately suppressed by treatment. Worldwide, for every two individuals starting treatment, three are newly infected. While there’s no doubt that we’ve made tremendous progress in fighting the virus, we have a long way to go before the word “cure” is not taboo when it comes to HIV/AIDS.

    See the full article here.

    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.

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  • richardmitnick 1:46 pm on September 5, 2014 Permalink | Reply
    Tags: , , Medicine,   

    From PBS NOVA: “New Drug Clears Cancer Cells Through Immune System Judo” 

    PBS NOVA

    NOVA

    Fri, 05 Sep 2014
    Tim De Chant

    For years, scientists have been probing various immune response proteins in the hopes of finding a new way to target and destroy cancer cells. Yesterday, two months ahead of schedule, the FDA approved a drug that does just that, targeting the protein “programmed cell death 1,” or PD-1. While not the first drug to use the immune system to fight cancer, it may be the most promising to date.

    Pembrolizumab is currently approved for advanced melanoma patients who have no other treatment options left. In clinical trials, tumors shrank in 24% of patients, and in one particular trial, 69% of patients were alive after one year of pembrolizumab treatment, a number that shocked the doctors in charge.

    melanoma
    Melanoma cell

    Pembrolizumab works by suppressing the expression of PD-1. In a healthy cell, PD-1 is active and present on the surface of a cell. But when a cell is nearing the end of it’s life, PD-1 expression tapers off. Immune cells recognize this signal and come in to clear away the dead or dying cell. Researchers have discovered that, in many tumors, PD-1 continues to be expressed. By preventing PD-1 from appearing on the surface of a cell, they predicted that cancer cells would be eliminated by the body’s own defenses.

    Doctors are hopeful that therapies which target PD-1 will give patients new options with fewer side effects than traditional chemotherapy. Andrew Pollack, reporting for the New York Times:

    “This is really opening up a whole new avenue of effective therapies previously not available,” said Dr. Louis M. Weiner, director of the Georgetown Lombardi Comprehensive Cancer Center in Washington and a spokesman for the American Association for Cancer Research. “It allows us to see a time when we can treat many dreaded cancers without resorting to cytotoxic chemotherapy.”

    Pembrolizumab is being marketed as Keytruda by Merck, the drug’s developer. Priced at $12,500 per month or $150,000 per year, the drug is apparently more expensive than other cancer drugs. Pollack reports that some cancer doctors have expressed concern that the high price tag will be too dear for some patients.

    Pembrolizumab is an antibody that specifically targets PD-1, so side effects tend to be less severe than with more general chemotherapy. Patients still run the risk of a potentially harmful inflammatory response—a sign of a runaway immune system, though most tolerated the drug well.

    For now, pembrolizumab is limited to patients with advanced melanoma that doesn’t respond to other treatments, but Merck has seen promising results with lung and kidney cancers. Other pharmaceutical companies are racing to get their PD-1 drugs approved, too. As more drugs come on the market, and new ones are calibrated for different cancers, the next few years could be the beginning of a new era in clinical cancer treatments.

    See the full article here.

    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.

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  • richardmitnick 2:39 pm on September 2, 2014 Permalink | Reply
    Tags: , Autism, Medicine,   

    From Princeton: “Early cerebellum injury hinders neural development, possible root of autism, theory suggests” 

    Princeton University
    Princeton University

    September 2, 2014
    Morgan Kelly, Office of Communications

    A brain region largely known for coordinating motor control has a largely overlooked role in childhood development that could reveal information crucial to understanding the onset of autism, according to Princeton University researchers.

    The cerebellum — an area located in the lower rear of the brain — is known to process external and internal information such as sensory cues that influence the development of other brain regions, the researchers report in the journal Neuron. Based on a review of existing research, the researchers offer a new theory that an injury to the cerebellum during early life potentially disrupts this process and leads to what they call “developmental diaschisis,” which is when a loss of function in one part of the brain leads to problems in another region.

    cere
    Drawing of the human brain, showing cerebellum and pons

    The researchers specifically apply their theory to autism, though they note that it could help understand other childhood neurological conditions. Conditions within the autism spectrum present “longstanding puzzles” related to cognitive and behavioral disruptions that their ideas could help resolve, they wrote. Under their theory, cerebellar injury causes disruptions in how other areas of the brain develop an ability to interpret external stimuli and organize internal processes, explained first author Sam Wang, an associate professor of molecular biology and the Princeton Neuroscience Institute (PNI).

    wang
    Princeton University researchers offer a new theory that an early-life injury to the cerebellum disrupts the brain’s processing of external and internal information and leads to “developmental diaschisis,” wherein a loss of function in one brain region leads to problems in another. Applied to autism, cerebellar injury could hinder how other areas of the brain interpret external stimuli and organize internal processes. Based on a review of existing research, the researchers found that a cerebellar injury at birth can make a person 36 times more likely to score highly on autism screening tests, and is the largest un-inherited risk (above).

    “It is well known that the cerebellum is an information processor. Our neocortex [the largest part of the brain, responsible for much higher processing] does not receive information unfiltered. There are critical steps that have to happen between when external information is detected by our brain and when it reaches the neural cortex,” said Wang, who worked with doctoral student Alexander Kloth and postdoctoral research associate Aleksandra Badura, both in PNI.

    “At some point, you learn that smiling is nice because Mom smiles at you. We have all these associations we make in early life because we don’t arrive knowing that a smile is nice,” Wang said. “In autism, something in that process goes wrong and one thing could be that sensory information is not processed correctly in the cerebellum.”

    Mustafa Sahin, a neurologist at Boston’s Children Hospital and associate professor of neurology at Harvard Medical School, said that Wang and his co-authors build upon known links between cerebellar damage and autism to suggest that the cerebellum is essential to healthy neural development. Numerous studies — including from his own lab — support their theory, said Sahin, who is familiar with the work but was not involved in it.

    “The association between cerebellar deficits and autism has been around for a while,” Sahin said. “What Sam Wang and colleagues do in this perspective article is to synthesize these two themes and hypothesize that in a critical period of development, cerebellar dysfunction may disrupt the maturation of distant neocortical circuits, leading to cognitive and behavioral symptoms including autism.”

    Traditionally, the cerebellum has been studied in relation to motor movement and coordination in adults. Recent studies, however, strongly suggest that it also influences childhood cognition, Wang said. Several studies also have found a correlation between cerebellar injury and the development of a disorder in the autism spectrum, the researchers report. For instance, the researchers cite a 2007 paper in the journal Pediatrics that found that individuals who experienced cerebellum damage at birth were 40 times more likely to score highly on autism screening tests. They also reference studies in 2004 and 2005 that found that the cerebellum is the most frequently disrupted brain region in people with autism.

    “What we realized from looking at the literature is that these two problems — autism and cerebellar injury — might be related to each other” via the cerebellum’s influence on wider neural development, Wang said. “We hope to get people and scientists thinking differently about the cerebellum or about autism so that the whole field can move forward.”

    The researchers conclude by suggesting methods for testing their theory. First, by inactivating brain-cell electrical activity, it should be possible to pinpoint the developmental stage in which injury to one part of the brain affects the maturation of another. A second, more advanced method is to reconstruct the neural connections between the cerebellum and other brain regions; the federal BRAIN Initiative announced in 2013 aims to map the activity of all the brain’s neurons. Finally, mouse brains can be used to disable and restore brain-region function to observe the “upstream” effect in other areas.

    The paper, The cerebellum, sensitive periods, and autism,” was published Aug. 6 in Neuron. The work was supported by grants from the National Institutes of Health (grant nos. R01 NS045193 and F31 MH098651), the Nancy Lurie Marks Family Foundation, and the Sutherland Cook Fund.

    See the full article here.

    About Princeton: Overview

    Princeton University is a vibrant community of scholarship and learning that stands in the nation’s service and in the service of all nations. Chartered in 1746, Princeton is the fourth-oldest college in the United States. Princeton is an independent, coeducational, nondenominational institution that provides undergraduate and graduate instruction in the humanities, social sciences, natural sciences and engineering.

    As a world-renowned research university, Princeton seeks to achieve the highest levels of distinction in the discovery and transmission of knowledge and understanding. At the same time, Princeton is distinctive among research universities in its commitment to undergraduate teaching.

    Today, more than 1,100 faculty members instruct approximately 5,200 undergraduate students and 2,600 graduate students. The University’s generous financial aid program ensures that talented students from all economic backgrounds can afford a Princeton education.

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  • richardmitnick 2:05 pm on September 2, 2014 Permalink | Reply
    Tags: , , , Medicine   

    From Carnegie Mellon: “Acoustic Tweezers” 

    Carnegie Mellon University logo
    Carnegie Mellon university

    Carnegie Mellon University President Subra Suresh and researchers from MIT and Pennsylvania State University have devised a new way to separate cells by exposing them to sound waves as they flow through a tiny channel.

    five
    [l-r] Tony Huang, Ming Dao, Subra Suresh, Peng Li, Zhangli Peng

    Their device could be used to detect the extremely rare tumor cells that circulate in cancer patients’ blood, helping doctors predict whether a tumor is going to spread.

    no

    “The method we describe in this paper is a step forward in the detection and isolation of circulating tumor cells in the body,” Dr. Suresh said. “It has the potential to offer a safe and effective new tool for cancer researchers, clinicians and patients.”

    The research is published online in the Proceedings of the National Academy of Sciences (PNAS).

    The paper describes a process that could dramatically alter the way scientists on the leading edge of cell research, disease diagnostics and therapeutics conduct their work. The technology demonstrated can be used to separate rare circulating cancer cells from white blood cells. The researchers have filed for a patent on the device.

    The method used by President Suresh and his co-authors shows unique promise. It causes the least disturbance and damage to the cells being separated of any process developed so far.

    Their approach adopts a method that researchers sometimes call “acoustic tweezers.”

    “Acoustic pressure is very mild and much smaller in terms of forces and disturbance to the cell,” said Ming Dao, a principal research scientist in MIT’s Department of Materials Science and Engineering and one of the senior authors of the paper.

    Dao said this is a gentler method to existing cell-sorting technologies, which require tagging the cells using chemicals or exposing them to damaging mechanical forces.

    The team was able to accurately separate cells when the difference between cell diameters was smaller than two micrometers.

    Dao said that the next steps are to test the device using patient samples and improve the throughput to shorten the process time.

    “When blood is out of the body too long, the properties change,” Dao said.

    Tony Jun Huang, a professor of engineering science and mechanics at Penn State, is also a senior author of the paper. Lead authors are MIT postdoc Xiaoyun Ding and Zhangli Peng, a former MIT postdoc who is now an assistant professor at the University of Notre Dame.

    See the full article here.

    Carnegie Mellon University (CMU) is a global research university with more than 12,000 students, 95,000 alumni, and 5,000 faculty and staff.
    CMU has been a birthplace of innovation since its founding in 1900.
    Today, we are a global leader bringing groundbreaking ideas to market and creating successful startup businesses.
    Our award-winning faculty members are renowned for working closely with students to solve major scientific, technological and societal challenges. We put a strong emphasis on creating things—from art to robots. Our students are recruited by some of the world’s most innovative companies.
    We have campuses in Pittsburgh, Qatar and Silicon Valley, and degree-granting programs around the world, including Africa, Asia, Australia, Europe and Latin America.

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