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  • richardmitnick 2:43 pm on December 5, 2016 Permalink | Reply
    Tags: , , Chemotherapy can cause metastasis, , Prof. Yuval Shaked,   

    From Technion via Globes: “Research: Chemotherapy can cause metastasis” 

    Technion bloc

    Technion

    1

    Globes

    5 Dec, 2016
    Gali Weinreb

    2
    Prof. Yuval Shaked

    New research at Israel’s Technion alarmingly reveals that the body acts to assist the tumor because it wrongly identifies chemotherapy as damaging.

    New research at Israel’s Technion alarmingly reveals that the body acts to assist the tumor because it wrongly identifies chemotherapy as damaging.

    As if the pressure caused by chemotherapy treatment was not enough, the results of the research conducted by Prof. Yuval Shaked may provide a new cause for alarm: in a series of research studies on animals, human cancer tumor cultures and indirectly also on cancer patients themselves, Shaked and his team found that while chemotherapy destroys the tumor, it encourages the development of metastasis tumors. This takes place since the body identifies chemotherapy as an attack on the body itself and mobilizes all systems for the least desirable cause – saving the tumor. At the same time, Shaked, a researcher at the new Technion Integrative Cancer Research Center, is quick to clarify: “Our research studies do not imply that chemotherapy treatments should be stopped. Chemotherapy still does more good than harm.”

    What does this series of research studies say? It identifies a real need to find a new solution, in which chemotherapy is applied in a way that reduces the damage caused as much as possible, while preserving its benefits. And Shaked also has some relevant ideas, presented in his research.

    “This series of research studies began years ago. It has been known and evident for years that cancer tumors become resistant to chemotherapy and turn ever more aggressive over time, but estimates had been that this entire development takes place inside the cancer cells themselves, the cells that remained in the body despite the damage of chemotherapy,” Shaked explains. “Following our research, it appears that the reality is somewhat more complex. It seems that resistance is developed not only by tumor cells, but by the patient’s entire body. Resistance to the treatment is directed by the body.”

    When the tumor sustains damage, body systems wrongly identify it as undesired damage to the body and act to assist the tumor. And there is even worse news: “This is true not only for chemotherapy, but for any intervention aimed at damaging the tumor. Once the tumor is harmed, the body tries to help,” Shaked says.

    The mechanisms to treat this damage do not only cause renewed multiplication in cancer tumor cells, after chemotherapy has caused it to shrink, they also turn it more violent and aggressive and encourage the formation of metastasis tumors. Animal trials have shown that even if there are no tumors, the provision of chemotherapy or anticancer drugs that kill cells activate damage treatment mechanisms that could stir cancerous processes in a mouse, if they already existed.

    In order to further support their conclusion, Shaked and his team conducted a third test in which they first treated healthy mice with an anticancer drug (not chemotherapy, but a new generation drug) such as Velcade, and only later infected the mice with cancer, without treating them. The mice treated with Velcade before infection died earlier than mice that had not been treated.

    So, the resistance of cancer to treatment, the fact that treatment becomes less effective over time, is caused by the body and not the cancer cells themselves.

    “The cancer cell and the tumor probably also have some resistance, but articles have been published saying that this resistance alone does not always explain the tumor returning after the treatment; that is, this cannot happen so rapidly only via evolution and selection of tumor cells, and there is another explanation.”

    After their research on animals, in which Shaked and his team have shown that mice treated with chemotherapy developed more metastasis tumors, with tumors becoming more aggressive, and following the research indicating that treatment alone is harmful to an animal that had no cancer to begin with, further human research studies have been conducted.

    “We took blood samples from a patient before and after chemotherapy treatment and dripped it on cancer cells in a dish. The cells that encountered the blood of a patient who had been treated with chemotherapy turned more aggressive. The blood contained materials that encouraged the development of the main tumor, and probably also of metastasis tumors.”

    Then why continue with chemotherapy anyway?

    “Despite our findings, these are the best treatments available today. The advantages of destroying the tumor using chemotherapy, which extends the patient’s life, at present outweigh the harm caused by bolstered resistance and metastasis tumors. As mentioned, this is true not only for chemotherapy treatment, but for any treatment that damages the tumor and causes it to develop resistance.”

    But what about the test you have presented, in which mice that received Velcade and were infected with cancer had lived for a shorter period than mice only infected with cancer?

    “These were mice that first received Velcade, and only after the body started secreting materials encouraging damage repair, which we already know also encourage metastasis and make the tumor more aggressive – only then were they infected with cancer, without receiving any treatment. If, after infection, we would have continued treating the mouse with Velcade, I believe that it would have still lived longer than the mice that received no treatment.”

    Does this mean that drug treatment should be continued – always and without any reservations?

    “This is not something I can answer in a sweeping manner. Every patient should consult their doctor. In the future, we might be able to predict which patients will develop a strong bodily reaction to the treatment, which will encourage the tumor to a greater extent, and for whom chemotherapy is not advisable, and who will have a weak reaction, turning this into a worthwhile treatment.”

    A cause for optimism

    After Shaked has shown the potential damage (as well as the usefulness) of cancer treatments, he has started examining ways of reducing this damage and turning the treatments more effective.

    In order to do this, you need to first understand how exactly the treatment affects the body.

    “We have estimated that the mechanism also involves the immune system, and therefore conducted another experiment: we took cells from the immune system of an animal and subjected them to chemotherapy. We have discovered that the process does pass through immune system cells. When we returned these immune cells to a mouse that did not undergo the treatment but has cancer, it was as if the mouse himself received the treatment – the increased aggressiveness of the tumor of the mouse that did not undergo the treatment but was injected with cells from the immune system of a mouse that did undergo the treatment resembled that of a mouse that did undergo the treatment.

    “So what is the cause for optimism? The next test: we took immune system cells, exposed them to chemotherapy, but this time with a drug that prevents the learning process that helps repair the damage. This time, when we injected the cells back to a mouse sick with cancer, his condition did not deteriorate.

    “Looking 800 steps ahead, if we could provide a person undergoing chemotherapy with a drug that could prevent his immune system from becoming accustomed to chemotherapy, the body may not develop the response which assists the tumor, and the tumor may not become so resilient or aggressive, which would make chemotherapy significantly more effective. Some of the drugs preventing the immune system from becoming accustomed to chemotherapy already exist and are sometimes given to patients with various illnesses (not necessarily cancer); they can be converted into cancer treatment quite easily.”

    You have mentioned the body’s reaction to chemotherapy can differ between patients.

    “We have so far discovered about 60 different factors in the body which are affected by chemotherapy; their combination affects the tumor and the metastasis reaction. These 60 factors are in fact 60 new targets for anti-cancer drugs, 60 factors that can be affected by drugs to reduce the reaction. There are already drugs on the market that could affect some of these factors. For example, we found an arthritis drug which reduces one of these harmful factors (that is, factors helping the tumor), and we have indeed shown that if it is provided with chemotherapy to mice with cancer, some of them have a longer life expectancy.

    “We could theoretically, create a combination matched to every patient, which depends on which of these 60 factors are affected by chemotherapy for that specific patient. These combinations could reduce pro-cancer reactions and thereby extend the patient’s life.”

    In the search for a cure for cancer, the body’s reaction to the cure is not even examined today, but only the treatment’s efficacy, right?

    “In principle, you are correct, other than one comment – in addition to testing the cure’s effectiveness in shrinking the tumor, the extent to which the drug is toxic to the body and the patient is also tested; but the body’s other reactions, which could eventually help the cancer cells are never examined. The main insight from our research is that the body does dictate the future of the tumor. The result of the treatment follows from the interaction between the treatment itself, the type of the treatment, and the specifics of the patient’s body.”

    One of the findings of Shaked’s research is that not only chemotherapy, but any damage to a cancerous cells creates a pro-cancerous counter-reaction in the body, but he says that there are also exceptions. “There is a certain type of chemotherapy, or more correctly a certain regimen, which we found does not result in a negative reaction in the body,” he says and explains: “At present, when administering chemotherapy, the principle is to bombard the body with the largest dosage of the material that can be administered without killing the patient. This method makes a lot of sense, since it provides for the most probable destruction of the tumor. Therefore, according to the logic that has guided the medical world so far, it verifies that nothing is left of the tumor, thereby reducing the chances of it recurring. However, our research indicates that it is exactly such chemotherapy treatment, a maximum-dosage ‘bombardment’, which creates the body’s counter-reaction that encourages tumor aggressiveness. This is of course not the only problem with high-dosage chemotherapy. It causes numerus side effectives and immense damage to the patient. After completing a high-dosage chemotherapy, the body must be given time to recover, which also gives the tumor time to recover.

    At present, with no relation to our research, they have begun testing a treatment method called metronomic chemotherapy on patients, a ‘continuously-administered’ treatment. The intention is to provide small doses of chemotherapy, but administer them on a daily basis. This dosage results in fewer side effects and enables the patient to continue with his daily life. As a result, the tumor does not shrink much, but also does not grow much, or at least, if it does grow, it does so slowly. A cancerous tumor that lives in the body and does not grow does not damage the patient. Only once it starts growing in a more significant manner does it damage other tissue and consume body resources in ways that are harmful. If a metronomic treatment enables patients to live with the same tumor for a long time, without completely killing it but exerting some control, as done with other chronic diseases, and while maintaining a good quality of life, it might be preferable to bombardment.

    “It is very important to remain cautious when discussing this possibility, since this is still an experimental treatment. It is currently undergoing phase III human trials. So far, the results show that with some patients, already subjected to many other treatments, who have developed resistance to everything and have had no other alternative, life expectancy has been extended using low-dosage chemotherapy treatment. This is a generic drug which is not at expensive.”

    Shaked says that the metronomic method raises concerns among most doctors, since it contradicts everything they have learned about proper chemotherapy, “but for patients with no proper treatment alternatives, this is certainly a possibility that should be examined.”

    Shaked adds that an initial examination run by him and his team raised the possibility that such a treatment, with a small daily dosage, causes the body to react less than a classic chemotherapy regimen, thereby keeping the tumor less aggressive for a longer period. But, for the time being, these are only assumptions. “We are currently running a test aimed at discovering the chemotherapy dosage that does not cause a negative body reaction,” he says.

    “One of the problems with such a treatment is that only a few chemotherapy drugs can be administered orally. A daily infusion is not a viable solution and producing a chemotherapy pump is impossible, which the agent will damage subdermal tissue in the place where the pump is injected. In order to make such a treatment succeed on the market, we will have to develop new chemotherapy formulas, which can be administered orally.

    “This is not necessarily a bad thing; while old-school chemotherapy is no longer patented and therefore drug companies have little motivation to research and develop it, such a drug, with an innovative drug administration mechanism, would be patented, making it more lucrative for drug companies.”

    See the full article here .

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    Stem Education Coalition

    Technion Campus

    A science and technology research university, among the world’s top ten,
    dedicated to the creation of knowledge and the development of human capital and leadership,
    for the advancement of the State of Israel and all humanity.

     
  • richardmitnick 1:51 pm on December 5, 2016 Permalink | Reply
    Tags: An X-Ray Surprise! When Black Holes Stop Eating Galaxies Fade Away, , ,   

    From Ethan Siegel: “An X-Ray Surprise! When Black Holes Stop Eating, Galaxies Fade Away” 

    From Ethan Siegel

    Dec 5, 2016

    1
    The optical/radio and X-ray emissions of Markarian 1018, which brightened in the 1980s and has faded in the 2010s. Image credit: X-ray: NASA/CXC/Univ of Sydney/R.McElroy et al, Optical: ESO/CARS Survey.

    Most large galaxies are illuminated by billions of stars, but some cosmic monstrosities have an even greater source of light: an active, supermassive, feeding black hole.

    2
    The active supermassive black hole at the center of galaxy Centaurus A produces two massive, bipolar jets in opposite directions. Image credit: NASA/CXC/CfA/R. Kraft et al.

    They outshine all others in terms of brightness, and show unique signs over the entire electromagnetic spectrum.

    3
    The looping, swirling filaments of the galaxy at the heart of the Centaurus cluster were shocked by central emissions. Someday, they may yet be devoured by the black hole. Image credit: NASA, ESA/Hubble, A. Fabian.

    Physically, the intense outburst heats up and shocks the surrounding matter as the black hole devours matter.

    4
    The galaxy NGC 1275, as imaged by Hubble, shows incredible signs of an active, feeding black hole at its center. Image credit: NASA, ESA, and the Hubble Heritage (STScI/AURA)-ESA/Hubble Collaboration.

    After the black hole stops feeding, some intense emission remains, even extending beyond the galaxy’s stars.

    5
    The bright emissions extending past the edge of the galaxies are evidence of prior AGN activity, but the central black holes are too dim now. Image credit: NASA / ESA / W. Keel, University of Alabama.

    The orientation of an active galactic nucleus determines what we observe, but they’re fundamentally a single class of object.

    6
    The unified model of AGNs/Active Galactic Nuclei. Image credit: Robert Antonucci, aka Ski, of http://web.physics.ucsb.edu/~ski/skipicture-1.html.

    For the first time, we’ve witnessed a single galaxy brighten and fade in detail: from inactive to active and back.


    Access mp4 video here .

    This galaxy in the constellation of Cetus, Markarian 1018, was viewed across the electromagnetic spectrum.

    8
    The galaxy Markarian 1018, at the center of a wide-field image from the Digitized Sky Survey. Image credit: ESO/Digitized Sky Survey 2. Acknowledgement: Davide De Martin, edits by E. Siegel.

    9
    Data from Chandra and other telescopes suggest that the supermassive black hole within this galaxy is no longer being fed enough fuel to make its surroundings shine brightly. Image credit: NASA/CXC/Univ of Sydney/R.McElroy et al.

    But it’s the X-rays, from Chandra, that are most revealing: dimming by a factor of 8 from 2010 to 2016.

    10
    Optical image of galaxy Markarian 1018, with an overlay of VLT (radio) data. Image credit: ESO/CARS Survey.

    Starve the black hole, and your galaxy dims. An incredible cosmic lesson that we’ve now seen firsthand!

    See the full article here .

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    “Starts With A Bang! is a blog/video blog about cosmology, physics, astronomy, and anything else I find interesting enough to write about. I am a firm believer that the highest good in life is learning, and the greatest evil is willful ignorance. The goal of everything on this site is to help inform you about our world, how we came to be here, and to understand how it all works. As I write these pages for you, I hope to not only explain to you what we know, think, and believe, but how we know it, and why we draw the conclusions we do. It is my hope that you find this interesting, informative, and accessible,” says Ethan

     
  • richardmitnick 1:06 pm on December 5, 2016 Permalink | Reply
    Tags: , , Gene Therapies for Fatal Diseases, , Ronald G. Crystal   

    From Cornell: “Gene Therapies for Fatal Diseases” 

    Cornell Bloc

    Cornell University

    12.5.16
    Caitlin Hayes

    Ronald Crystal is known for developing a treatment for a common, often-fatal hereditary disorder that causes emphysema and liver disease.

    1
    Ronald Crystal. No image credit.

    In the 1980s, Ronald G. Crystal, Chairman, Department of Genetic Medicine, Weill Cornell Medicine, developed a treatment for one of the most common hereditary disorders in Caucasians: Alpha-1 Antitrypsin (A1AT) Deficiency. The inability to produce normal levels of the A1AT protein makes patients susceptible to emphysema and liver disease and is often fatal. Crystal and his team were able to purify the deficient protein from normal blood samples and deliver it back to patients with the disorder. More than 6,000 people around the world are using this treatment today, but Crystal says there’s a catch.

    “Proteins have a very short half-life,” he says. “For A1AT, they last about one week, so you have to administer the therapy with intravenous infusions every week.”

    n 1989 with prompting from a former postdoctoral student and collaborator, Crystal saw an opportunity to develop a one-time treatment for A1AT deficiency. By using a virus to deliver the gene that produces the protein, researchers could in theory give a patient the lifelong machinery to make their own A1AT. “It was this eureka moment of realizing that if we had the right virus, we might be able to take a hereditary disorder and use the virus one time to cure the disease,” says Crystal. “That’s what got me started on gene therapy.”

    Gene Therapies, Licensed and Ready for Clinical Trials

    Almost 30 years and many contributions later, Crystal may finally have the gene therapy for A1AT deficiency that would require just one dose. He licensed this technology, along with two other therapies, to a startup he co-founded in 2014, Annapurna Therapeutics. Annapurna recently merged with another company to form Adverum Biotechnologies, which will independently carry out a large clinical trial of Crystal’s gene therapy for A1AT deficiency. Crystal is an advisory board member and a paid consultant for Adverum.

    The Technology—How It Works

    Crystal’s lab focuses on in vivo gene therapy, whereby genes are delivered directly to the patient. “The problem and the challenge of the technology has been how do you get genes into human cells? How do you get them to go where you want them to go?”

    The answer is viruses. Viruses have evolved to transfer their genetic material to the cell, usually to the nucleus, and they can target certain organs or tissues. Once there, “they basically hijack the cell’s genetic machinery to reproduce themselves,” Crystal explains. In the gene therapy field, researchers essentially empty these viruses of their own genetic information and replace it with genes that a patient needs expressed.

    “We use the structure of the virus like a Trojan horse,” Crystal says. “The idea is then to directly administer the virus to the brain or heart or liver, and the virus will deliver the genetic information to the nucleus of the cell. There, it uses the cell’s genetic machinery to transcribe the gene, make a protein, and then that protein either functions within the cell or is secreted.”

    A good deal of the work in Crystal’s lab therefore involves finding and modifying viruses and genes for target organs, inserting therapeutic genes into viruses, and carrying out the studies in animal models and in small clinical trials. The therapies licensed to Adverum include the A1AT deficiency therapy as well as a therapy for another genetic disorder: hereditary angioedema. In patients with hereditary angioedema, blood vessels leak fluid and cause excessive swelling, which can lead to premature death. The third treatment is a gene therapy for severe allergy such as peanut allergy. “We can cure the diseases in mouse models in one dose,” says Crystal. “Whether they’ll work in humans, of course, we don’t know—yet.”

    The Partnership of Academia and Industry for Conducting Large-Scale Clinical Trials

    When it comes to the kinds of large-scale clinical trials that are necessary for drug approval, academics often don’t have the resources, Crystal says. “In the academic world, we can carry out early phase I studies, studies in 20 or 30 patients, but we don’t have the infrastructure or the funds to carry out the large studies that are required.”

    One answer is to partner with biotech and pharmaceutical companies, Crystal continues. “In our lab, we’ve made the initial viruses, shown that they work in animal models, in some cases shown safety, in some cases not yet,” he explains. “The concept then is to partner the academic environment—with new ideas, new therapies, and early data—with industry. They will take it over and run the clinical trials, and turn it into a drug if it works.”

    To avoid conflicts, Crystal won’t be involved in the clinical trials. “I think it’s a very good paradigm, a good way that we in the academic world can get the ideas and the creativity that we have and move it towards curing patients.”

    Foresight: Linking Technologies to Clinical Problems

    As a pulmonary doctor by training, Crystal has always had an eye on clinical problems and how his research can address them. When he began working in the gene therapy field, he followed the technology to the problems that this technology could address.

    “It’s really a kind of opportunism, in terms of understanding how the technology can be married to a clinical problem,” he says. “It’s a combination of seeing the advantages and limitations to the technology and being lucky enough to have training in medicine—so we can see how to use this technology and where best to apply it.”

    While the technology has guided Crystal to certain problems, the underlying goal has always been to improve human health. At the National Institutes of Health, where he worked for 23 years before joining Weill Cornell Medicine, his group was the first to carry out a human gene therapy in vivo to treat cystic fibrosis. With his collaborators, he has also worked on therapies for cardiac ischemia, cancer, and central nervous system disorders, and he is developing vaccines for addictive substances such as cocaine as well as other projects.

    Fusing Basic Science and Clinical Medicine

    “I decided a long time ago to focus my career on that interface between basic science and clinical medicine,” Crystal says. “I think if you ask my colleagues, physician-scientists who do similar kinds of things, probably the most satisfying thing is to at least have the opportunity to develop therapies for human disease. When we can do something and play a role in its success, that’s very satisfying.”

    Weill Cornell Medicine, Crystal continues, is a great place for the kind of work that brings basic science to clinical problems. “As a clinical scientist, it’s very important to have access to individuals who are willing to participate in clinical trials, and 10 percent of the population lives within 50 miles of Weill Cornell Medicine,” he explains, “and we have Weill Cornell Medicine, The Rockefeller University, Memorial Sloan Kettering Cancer Center, Hospital for Special Surgery—it’s a very high density of clinical and scientific talent. That’s a wonderful milieu to be in.”

    See the full article here .

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

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

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

     
  • richardmitnick 12:40 pm on December 5, 2016 Permalink | Reply
    Tags: , Mukesh Patel, Rutgers Honors College   

    From Rutgers: “Innovation Laboratory at Rutgers’ Honors College Teaches Students How to Bring Ideas to Life” 

    Rutgers University
    Rutgers University

    December 5, 2016
    Jeff Tolvin
    jeff.tolvin@rutgers.edu
    908-229-3475

    Six proposals, from a pacifier that can deliver nutrients to newborns to a Bluetooth device to help prevent sexual assault, are in incubation stage this year.

    1
    Mukesh Patel, who has helped many startup companies develop their business plans, is the inaugural director of innovation of the Honors College. Photo: Jeff Tolvin

    Mukesh M. Patel, a successful entrepreneur, mentor, business attorney and adjunct professor at Rutgers Business School and Rutgers School of Law who has helped many startup companies develop their business plans and raise significant equity funding, heads the Innovation Lab at the Honors College at Rutgers University-New Brunswick. He joined the college as its inaugural director of innovation this past summer.

    The Honors College incorporated the Innovation Lab into its curriculum to enable students to collaborate across disciplines and tackle complex and global problems in tangible ways.

    The Honors College mission course, “the Forum,” challenges first-year students to come up with ideas for innovations that could solve societal issues and become sustainable, profitable ventures. Of the more than 100 ideas pitched last year, six advanced to become the focus for hands-on development in the Innovation Lab by second-year students.

    Rutgers Today recently spoke with Patel about how the Innovation Lab is designed to work and the student projects in development.

    What is the Innovation Lab?

    Patel: First, it is a physical space where students of different disciplines and passions come together to develop their ideas. By its design, the lab avoids silos and breaks down boundaries. We call the process “design-thinking,” and it’s what occurs when teams work collaboratively on projects small or large. We have equipment, such as 3-D printers, mini-computers with a digital design studio, sensor lab, and other gadgetry to test hypotheses, create prototypes and minimally viable products (MVPs) and run pilot programs.

    Conceptually, the lab represents how Honors College students learn critical skills vital to developing and bringing an idea to market. This includes how to recruit students from the university because of the expertise they could contribute, plus marketing, public relations and concept testing.

    What are the projects under development in the Innovation Lab this year?

    Patel: The projects include RFInD, a wearable electronic device programmed with personal medical information to help emergency health care providers find and treat patients in distress; eUse-IT, a system for collecting and repairing laptop computers to reduce electronic waste while making computer devices more accessible to lower-income demographics; Nutrivide, a device resembling a pacifier that provides nutrients to undernourished newborns; Oasis, a process for delivering nutritious food to needy communities and food deserts; Exalight, a specially-designed blanket to prevent neonatal jaundice and potentially treat certain skin conditions; and Merakhi, a Bluetooth and audio wearable tech device to help prevent sexual assault while providing education and empowerment in connection with rape and assault cultures.

    What are the tangible goals of the Innovation Lab?

    Patel: We teach students how to build an entrepreneurial ecosystem. We expose them to the resources and the basics of building a project through a series of learning opportunities: lectures, discussions, debates and practical workshops throughout the tri-state area. Students attend at least 10 events that revolve around four themes: innovation, startups, social ventures and social impact. We teach them how to raise capital, how to adapt a product idea to fit a need (product-market fit) and how to become inspired about a project while learning how to lead and inspire team collaboration.

    We expose them to CEOs and top executives of public and private companies and thought leaders and how to work with other startups. They may also use laboratories at other institutions or businesses, wherever they determine they can receive assistance in developing their venture. We are planning field trips to, and exploring opportunities for collaboration with, business and engineering schools, innovation labs and entrepreneurship centers at other universities such as Princeton, Columbia, Harvard, MIT, NJIT, Stevens and Montclair State University.

    The Innovation Lab fellows will also compete in state, national and global venture competitions. In fact, in our first innovation competition run by the New Jersey Technology Council, two of our venture teams placed in the top position as finalists earning a $1,000 cash prize per team. In addition, two of the venture teams were accepted into the Rutgers Law School Entrepreneurship Clinic, where they qualify for complimentary legal services. Furthermore, all six venture teams were accepted to participate in the Social Entrepreneurship Venture Summit in New York City run by the KIND Foundation and Venture for America, where our students met with social innovators such as Daniel Lubetzky (founder and CEO of KIND Snacks and the KIND Foundation), Andrew Yang (founder and CEO of Venture for America), and Arianna Huffington (founder and CEO of Huffington Post and Thrive Global).

    What are the key lessons you want students to learn?

    Patel: We teach thought-leadership and stress the importance of not being afraid of failure, to push the boundaries. We emphasize exhausting all free resources before applying for the limited seed money available. We want students to learn what to do to advance a project resourcefully while applying lean methodologies.

    We want them to understand how, as 19-year-olds, they can have a significant impact on the world. That’s a big part of the process. They need to learn persistence and how to pivot; to go through the journey and experience the process. We want them to be inspired for what they want to do. We want their impact to be long-term.

    They are required to build an advisory board, but not only consisting of people they know. They start forming relationships and determining whatever the venture needs. This requires them to reach further. We want them to think that way. We want them to experience what to do when they are told “no.” The key is to teach them not to let obstacles get in the way of good ideas going forward. They learn and practice grit.

    How will you judge success of these projects?

    Patel: You can judge success in many ways. If you fail and nothing works, that could be a huge success because you took a huge risk, because you embraced failure, and hopefully learned from it. We say don’t be afraid of failure and to fail fast to succeed faster. A failure at one point could count as a success because that will mean you are one step closer to what might work.

    The more obvious success is something that becomes a national or global enterprise with a social impact, especially something with sustainability and profitability that creates opportunities to hire and create jobs.

    What drove you to accept the innovation position at the Honors College and how many ideas do you anticipate reaching production?

    Patel: As a Rutgers alumnus, I wanted to give back by engaging through designing and leading an innovative and creative platform for social impact. I was inspired by the opportunity to work with the top leaders at the Honors College who are catalysts, thought leaders, and game changers. They believed in and supported my vision and model to create something special, an experiential, collaborative, multi- and interdisciplinary ecosystem for impact through social innovation. I anticipate a significant percentage of the ideas will reach various phases of production, especially considering the creativity and drive of our students, the Innovation Lab fellows.

    See the full article here .

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    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.

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  • richardmitnick 12:19 pm on December 5, 2016 Permalink | Reply
    Tags: , , , ,   

    From Harvard Medical School: “Zika’s Entry Points” 

    Harvard University
    Harvard University

    harvard-medical-school-bloc

    Harvard Medical School

    December 1, 2016
    HANNAH ROBBINS
    ERIC BENDER

    Fast-spreading virus can take multiple routes into the growing brain.

    1
    Zika virus (light blue) spreads through a three-dimensional model of a developing brain. Image: Max Salick and Nathaniel Kirkpatrick/Novartis

    Around the world, hundreds of women infected with the Zika virus have given birth to children suffering from microcephaly or other brain defects, as the virus attacks key cells responsible for generating neurons and building the brain as the embryo develops.

    Studies have suggested that Zika enters these cells, called neural progenitor cells or NPCs, by grabbing onto a specific protein called AXL on the cell surface. Now scientists at the Harvard Stem Cell Institute (HSCI) and Novartis have shown that this is not the only route of infection for NPCs.

    The scientists demonstrated that the Zika virus infected NPCs even when the cells did not produce the AXL surface receptor protein that is widely thought to be the main vehicle of entry for the virus.

    “Our finding really recalibrates this field of research, because it tells us we still have to go and find out how Zika is getting into these cells,” said Kevin Eggan, principal faculty member at HSCI, professor of stem cell and regenerative biology at Harvard University’s Faculty of Arts and Sciences and Harvard Medical School, and co-corresponding author on a paper reporting the research in Cell Stem Cell.

    “It’s very important for the research community to learn that targeting the AXL protein alone will not defend against Zika,” agreed Ajamete Kaykas, co-corresponding author and a senior investigator in neuroscience at the Novartis Institutes for Biomedical Research (NIBR).

    Previous studies have shown that blocking expression of the AXL receptor protein does defend against the virus in a number of human cell types. Given that the protein is highly expressed on the surface of NPCs, many labs have been working on the hypothesis that AXL is the entry point for Zika in the developing brain.

    “We were thinking that the knocked-out NPCs devoid of AXL wouldn’t get infected,” said Max Salick, a NIBR postdoctoral researcher and co-first author on the paper. “But we saw these cells getting infected just as much as normal cells.”

    Working in a facility dedicated to infectious disease research, the scientists exposed two-dimensional cell cultures of AXL-knockout human NPCs to the Zika virus. They followed up by exposing three-dimensional mini-brain “organoids” containing such NPCs to the virus. In both cases, cells clearly displayed Zika infection. This finding was supported by an earlier study that knocked out AXL in the brains of mice.

    “We knew that organoids are great models for microcephaly and other conditions that show up very early in development and have a very pronounced effect,” said Kaykas. “For the first few months, the organoids do a really good job in recapitulating normal brain development.”

    Historically, human NPCs have been difficult to study in the lab because it would be impossible to obtain samples without damaging brain tissue. With the advancements in induced pluripotent stem cell (iPS cell) technology, a cell reprogramming process that allows researchers to coax any cell in the body back into a stem cell-like state, researchers can now generate these previously inaccessible human tissues in a petri dish.

    The team was able to produce human iPS cells and then, using gene-editing technology, modify the cells to knock out AXL expression, said Michael Wells, a Harvard postdoctoral researcher in the Eggan Lab and co-first author. The scientists pushed the iPS cells to become NPCs, building the two-dimensional and three-dimensional models that were infected with Zika.

    The Harvard and NIBR collaborators started working with the virus in mid-April 2016, only six months before they published their findings. This unusual speed of research reflects the urgency of Zika’s global challenge, as the virus has spread to more than 70 countries and territories.

    “At the genesis of the project, my wife was pregnant,” Eggan remarked. “One can’t read the newspapers without being concerned.”

    The collaboration grew out of interactions at the Broad Institute of Harvard and MIT’s Stanley Center for Psychiatric Research, where Eggan directs the stem cell program. His lab already had developed cell culture systems for studying NPCs in motor neuron and psychiatric diseases. The team at Novartis had created brain organoids for research on tuberous sclerosis complex and other genetic neural disorders.

    “Zika seemed to be a big issue where we could have an impact, and we all shared that interest,” Eggan said. “It’s been great to have this public/private collaboration.”

    The researchers are studying other receptor proteins that may be open to Zika infection in hopes that their basic research eventually will help in the quest to develop vaccines or other drugs that defend against the virus.

    See the full article here .

    YOU CAN HELP FIND A CURE FOR THE ZIKA VIRUS.

    There is a new project at World Community Grid [WCG] called OpenZika.
    Zika
    Zika depiction. Image copyright John Liebler, http://www.ArtoftheCell.com
    Rutgers Open Zika

    WCG runs on your home computer or tablet on software from Berkeley Open Infrastructure for Network Computing [BOINC]. Many other scientific projects run on BOINC software.Visit WCG or BOINC, download and install the software, then at WCG attach to the OpenZika project. You will be joining tens of thousands of other “crunchers” processing computational data and saving the scientists literally thousands of hours of work at no real cost to you.

    This project is directed by Dr. Alexander Perryman a senior researcher in the Freundlich lab, with extensive training in developing and applying computational methods in drug discovery and in the biochemical mechanisms of multi-drug-resistance in infectious diseases. He is a member of the Center for Emerging & Re-emerging Pathogens, in the Department of Pharmacology, Physiology, and Neuroscience, at the Rutgers University, New Jersey Medical School. Previously, he was a Research Associate in Prof. Arthur J. Olson’s lab at The Scripps Research Institute (TSRI), where he ran the day-to-day operations of the FightAIDS@Home project, the largest computational drug discovery project devoted to HIV/AIDS, which also runs on WCG. While in the Olson lab, he also designed, led, and ran the largest computational drug discovery project ever performed against malaria, the GO Fight Against Malaria project, also on WCG.

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    The Harvard Medical School community is dedicated to excellence and leadership in medicine, education, research and clinical care. To achieve our highest aspirations, and to ensure the success of all members of our community, we value and promote common ideals that center on collaboration and service, diversity, respect, integrity and accountability, lifelong learning, and wellness and balance. To be a citizen of this community means embracing a collegial spirit that fosters inclusion and promotes achievement.

    Harvard University campus

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

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

     
  • richardmitnick 10:27 am on December 5, 2016 Permalink | Reply
    Tags: , , , Kepler-11, The Sun has a new twin and its children are weird   

    From astrobites: “The Sun has a new twin, and its children are weird…” 

    Astrobites bloc

    Astrobites

    Dec 5, 2016
    David Wilson

    Article: Kepler-11 is a Solar Twin: Revising the Masses and Radii of Benchmark Planets Via Precise Stellar Characterization
    Authors: Megan Bedell, Jacob L. Bean, Jorge Melendez et al.
    First author’s institution: Department of Astronomy and Astrophysics, University of Chicago, USA.
    Status: Submitted to AAS journals

    1
    Figure 1: Artist’s schematic of the Kepler-11 system, compared with our own. Six planets tightly orbit a star, which today’s paper reveals to be almost identical to the Sun. Image credit: NASA.

    The current tally of known exoplanets stands at around three thousand, depending on who you ask. Among the hundreds of stars that these planets orbit, Kepler-11 is a standout case (it even has its own Wikipedia page). Kepler-11 has six planets, five of which would comfortably fit inside the orbit of Mercury (Figure 1). What’s more, all of the planets have remarkably low densities for their size. The tight orbits and low densities are contradictory: the planets must have thick gas atmospheres, but the star should have blown away all of the gas that close before the planets could form. As the planets are there despite this, the system provides an excellent test bed for planetary formation models.

    Today’s paper presents new observations of the central star of the Kepler-11 system. As nearly everything we know about exoplanets comes from measuring their effects on their host stars, detailed observations of those stars are necessary to fully understand the planets. Due to its faintness, however, previous observations of Kepler-11 are poor.

    To remedy this, Bedell et al. turned to one of the largest telescopes in the world, the twin ten-metre Keck telescopes on Mauna Kea, Hawaii.

    Keck Observatory, Mauna Kea, Hawaii, USA
    Keck Observatory Interior
    Keck Observatory, Mauna Kea, Hawaii, USA

    Over two nights, Keck stared at Kepler-11, along with nine stars that the authors thought might be similar to it. The telescopes produced spectra, splitting the light of each star into a rainbow of colours, complete with distinct imprints left by the chemicals in the stars’ atmospheres. As a comparison, the authors also obtained a spectrum of the Sun, using the light reflecting off the dwarf planet Ceres to avoid burning out the telescope.

    2
    Figure 2: Spectrum of Kepler 11, the Sun and one of the comparison targets. The bottom plot shows the differences between the spectra of the two stars and the Sun. In both plots, the near-match of Kepler-11 and the Sun can be clearly seen. Figure 1 from Bedell et al.

    The results showed that Kepler-11, despite having a planetary system utterly unlike the Solar system, is nearly identical to the Sun. Careful analysis of the spectrum showed that Kepler-11 and the Sun have almost exactly the same temperature, mass, and atmospheric chemistry. Bedell et al. point out that, unusually for spectra, the result can be seen by eye. Figure 2 shows the spectra of Kepler-11, the Sun and a comparison star, with Kepler-11’s line nearly tracing over the Solar spectrum.

    Kepler-11 is therefore placed firmly in the category of star known as “solar twin”. It isn’t quite an identical twin, being slightly younger and with a slightly more metal-rich atmosphere, but it’s very close. These twins are extremely useful for exoplanet studies, as comparing their planetary systems to our own can guide how we apply the lessons learnt about the planets here to more distant worlds.

    With that in mind, where do these new observations leave Kepler-11’s intriguing planetary system? As the mass and radii of the planets are measured in relation to the star, the new results for Kepler-11 mean that the planets’ characteristics also need revising.

    The authors find that the planets all must have higher masses than previously thought, as well as smaller radii. This means that the densities of the planets are about 30 percent higher than previously thought. They therefore need less gas to form, making their formation so close to the star a bit more believable. With the deluge of planet discoveries set to continue for years to come, Bedell et al. finish by pointing out the need for similar, high-quality studies of the stars of all of these new worlds.

    See the full article here .

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    What do we do?

    Astrobites is a daily astrophysical literature journal written by graduate students in astronomy. Our goal is to present one interesting paper per day in a brief format that is accessible to undergraduate students in the physical sciences who are interested in active research.
    Why read Astrobites?

    Reading a technical paper from an unfamiliar subfield is intimidating. It may not be obvious how the techniques used by the researchers really work or what role the new research plays in answering the bigger questions motivating that field, not to mention the obscure jargon! For most people, it takes years for scientific papers to become meaningful.
    Our goal is to solve this problem, one paper at a time. In 5 minutes a day reading Astrobites, you should not only learn about one interesting piece of current work, but also get a peek at the broader picture of research in a new area of astronomy.

     
  • richardmitnick 10:10 am on December 5, 2016 Permalink | Reply
    Tags: , , , ,   

    From COSMOS: ” ‘Locked, loaded and ready to roll’: San Andreas fault danger zones” 

    Cosmos Magazine bloc

    COSMOS

    05 December 2016
    Kate Ravilious

    1
    The Carrizo Plain in eastern San Luis Obispo County, California, contains perhaps the most strikingly graphic portion of the San Andreas fault. Roger Ressmeyer / Corbis / VCG

    A series of small earthquakes up to magnitude 4 started popping off right next to the San Andreas fault at the end of September, giving Californian seismologists the jitters.

    This swarm of more than 200 mini-quakes radiated from faults under the Salton Sea, right down at the southern end of the San Andreas fault.

    And although the small quakes only released tiny amounts of energy, the fear was that this fidgeting could be enough to trigger an earthquake on the big fault. “Any time there is significant seismic activity in the vicinity of the San Andreas fault, we seismologists get nervous,” said Thomas Jordan, director of the Southern California Earthquake Centre in Los Angeles.

    Because despite a plethora of sensitive instruments, satellite measurements and powerful computer models, no-one can predict when the next big one will rattle the Golden State.

    2
    Cosmos magazine / Getty Images

    Slicing through 1,300 kilometres of Californian landscape from Cape Mendocino in the north-west all the way to the Mexican border in the south-east, the San Andreas fault makes itself known.

    Rivers and mountain ranges – and even fences and roads – are offset by the horizontal movement of this “transform” fault, where the Pacific Ocean plate to the west meets the North American plate to the east. The fault moves an average of around 3.5 centimetres each year, but the movement comes in fits and starts. Large earthquakes doing most of the work, punctuating long periods of building pressure.

    The fault divides roughly into three segments, each of which tends to produce a big quake every 150 to 200 years.

    The last time the northern segment (from Cape Mendocino to Juan Bautista, south of San Francisco) released stress was during the devastating magnitude-7.8 San Francisco Bay quake in 1906, which killed thousands and destroyed around 80% of San Francisco.

    Meanwhile, the central section, from Parkfield to San Bernardino, has been quiet for longer still, with its last significant quake in 1857, when a magnitude-7.9 erupted underneath Fort Tejon.

    But most worrying of all is the southern portion (from San Bernardino southwards through the Coachella Valley), which last ruptured in the late 1600s. With more than 300 years of accumulated strain, it is this segment that seismologists view as the most hazardous.

    “It looks like it is locked, loaded and ready to roll,” Jordan announced at the National Earthquake Conference in Long Beach in May 2016.

    This explains why the recent earthquake swarm was considered serious enough for the United States Geological Survey to issue a statement: that the risk of a magnitude-7 quake in Southern California was temporarily elevated from a one in 10,000 chance to as much as a one in one in 100.

    “We think that such swarms of small earthquakes indicate either that fluids are moving through the crust or that faults have started to slip slowly,” says Roland Bürgmann, a seismologist at University of California, Berkeley. “There is a precedent for such events having the potential to trigger earthquakes.”

    And last year he showed it’s not just the San Andreas fault we need to worry about. Working near the northernmost segment of the fault, Bürgmann and his colleagues used satellite measurements and data from instruments buried deep underground to map out the underground shape of two smaller faults – the Hayward and Calaveras – which veer off to the east of San Francisco. These two smaller faults, which are known to be capable of producing their own sizeable earthquakes (up to magnitude 7), turned out to be connected [Geophysical Research Letters]. Until now, sediments smothered the link.

    And in October, another study published in Science Advances showed that the Hayward fault is connected by a similarly direct link to a third fault to the north – the Rodgers Creek fault.

    “This opens up the possibility of an earthquake that could rupture through this connection, covering a distance of up to 160 kilometres and producing an earthquake with magnitude much greater than 7,” Bürgmann says.

    “It doesn’t mean that this will happen, but it is a scenario we shouldn’t rule out.”

    Down the other end of the San Andreas fault, Julian Lozos from the California State University in Los Angeles has been testing various earthquake scenarios using a detailed computer model of the fault system.

    He too has shown that a seemingly minor side-fault – known as the San Jacinto – is more of a worry than previously thought. In this case, the San Jacinto falls short of intersecting the San Andreas by around 1.5 kilometres, but Lozos’ model suggests large earthquakes can leap this gap.

    “We already know that the San Andreas is capable of producing a magnitude-7.5 on its own, but the new possibility of a joint rupture with the San Jacinto means there are now more ways of making a magnitude-7.5,” says Lozos, whose findings were published in Science Advances in March this year.

    By feeding historic earthquake data into his model, he showed that the magnitude-7.5 earthquake that shook the region on 8 December 1812 is best explained by a quake that started on the San Jacinto but hopped across onto the San Andreas and proceeded to rupture around 50 kilometres north and southwards.

    If such a quake were to strike again today, the consequences could be devastating, depending on the rupture direction.

    “The shaking is stronger in the direction of unzipping,” explains Lozos. And in this case, the big worry is a northward unzipping, which would funnel energy into the Los Angeles basin.

    In 2008, the United States Geological Survey produced the ShakeOut Scenario: a model of a magnitude-7.8 earthquake, with between two and seven metres of slippage, on the southern portion of the San Andreas fault.

    Modern buildings could generally withstand the quake, thanks to strict modern building codes, but older buildings and any buildings straddling the fault would likely be severely damaged.

    But the greatest concern was the effect the movement would have on infrastructure – slicing through 966 roads, 90 fibre optic cables, 39 gas pipes and 141 power lines. Smashed gas and water mains would enable fires to rage, causing more damage than the initial shaking of the quake.

    The overall death toll was estimated at 1,800, and the long-term consequences expected to be severe, with people living with a sequence of powerful aftershocks, and a long slow road to recovery. Simply repairing water mains, for instance, could take up to six months.

    In this simulation, the city of Los Angeles doesn’t take a direct hit, since it lies some way from the San Andreas fault. But there is another scenario which keeps Jordan awake at night.

    Back in 1994, a magnitude-6.7 “Northridge” earthquake struck the San Fernando valley, about 30 kilometres north-west of downtown Los Angeles, killing 57 people and causing between US$13 and $40 billion of damage – the costliest natural disaster in the US at that time.

    3
    Collapsed overpass on Highway 10 in the Northridge/Reseda area – a result of the 1994 earthquake. Visions of America / UIG / Getty Images

    “This was a complete eye-opener for us all, as it occurred on a blind thrust fault that no-one knew existed,” says Jordan. Geologists have since worked overtime to discover these hidden faults, and in 1999 they found that Los Angeles itself sits atop the Puente Hills fault – a steeply angled “thrust” fault that is thought to produce earthquakes of greater than magnitude 7 every few thousand years.

    “We are more likely to see a large earthquake on the San Andreas fault in the short to medium term, but we still have to accept that this thrust fault could move at any time, and because of its location underneath Los Angeles, the consequences would be very severe,” says Jordan.

    Much of Los Angeles is underlain by soft sediments, which wobble furiously when rattled by a quake, and it is these areas that would likely sustain the most damage.

    Thankfully, the Los Angeles city council is taking the risk seriously. Models such as ShakeOut Scenario motivated the city to produce emergency plans and retrofit dangerous buildings. Seismologists such as Jordan and Lozos live in Los Angeles, but confess that the risk does affect their everyday life.

    “It crosses my mind when I drive over the freeway that collapsed in 1994, or when I’m deciding what kind of house to live in,” says Lozos. “Others mock me for worrying, but as a seismologist, I know that the longer you go without a quake the greater the chances of a quake are.”

    Meanwhile, Jordan, who lives in a house underlain by solid granite bedrock, justifies his decision to live in this precarious part of the world: “If you want to hunt elephants, you have to go to elephant country.”

    See the full article here .

    QCN bloc

    You can help catch earthquakes.

    Quake-Catcher Network

    The Quake-Catcher Network is a collaborative initiative for developing the world’s largest, low-cost strong-motion seismic network by utilizing sensors in and attached to internet-connected computers. With your help, the Quake-Catcher Network can provide better understanding of earthquakes, give early warning to schools, emergency response systems, and others. The Quake-Catcher Network also provides educational software designed to help teach about earthquakes and earthquake hazards.

    After almost eight years at Stanford, and a year at CalTech, the QCN project is moving to the University of Southern California Dept. of Earth Sciences. QCN will be sponsored by the Incorporated Research Institutions for Seismology (IRIS) and the Southern California Earthquake Center (SCEC).

    The Quake-Catcher Network is a distributed computing network that links volunteer hosted computers into a real-time motion sensing network. QCN is one of many scientific computing projects that runs on the world-renowned distributed computing platform Berkeley Open Infrastructure for Network Computing (BOINC).

    BOINCLarge

    BOINC WallPaper

    The volunteer computers monitor vibrational sensors called MEMS accelerometers, and digitally transmit “triggers” to QCN’s servers whenever strong new motions are observed. QCN’s servers sift through these signals, and determine which ones represent earthquakes, and which ones represent cultural noise (like doors slamming, or trucks driving by).

    There are two categories of sensors used by QCN: 1) internal mobile device sensors, and 2) external USB sensors.

    Mobile Devices: MEMS sensors are often included in laptops, games, cell phones, and other electronic devices for hardware protection, navigation, and game control. When these devices are still and connected to QCN, QCN software monitors the internal accelerometer for strong new shaking. Unfortunately, these devices are rarely secured to the floor, so they may bounce around when a large earthquake occurs. While this is less than ideal for characterizing the regional ground shaking, many such sensors can still provide useful information about earthquake locations and magnitudes.

    USB Sensors: MEMS sensors can be mounted to the floor and connected to a desktop computer via a USB cable. These sensors have several advantages over mobile device sensors. 1) By mounting them to the floor, they measure more reliable shaking than mobile devices. 2) These sensors typically have lower noise and better resolution of 3D motion. 3) Desktops are often left on and do not move. 4) The USB sensor is physically removed from the game, phone, or laptop, so human interaction with the device doesn’t reduce the sensors’ performance. 5) USB sensors can be aligned to North, so we know what direction the horizontal “X” and “Y” axes correspond to.

    If you are a science teacher at a K-12 school, please apply for a free USB sensor and accompanying QCN software. QCN has been able to purchase sensors to donate to schools in need. If you are interested in donating to the program or requesting a sensor, click here.

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

    Earthquake safety is a responsibility shared by billions worldwide. The Quake-Catcher Network (QCN) provides software so that individuals can join together to improve earthquake monitoring, earthquake awareness, and the science of earthquakes. The Quake-Catcher Network (QCN) links existing networked laptops and desktops in hopes to form the worlds largest strong-motion seismic network.

    Below, the QCN Quake Catcher Network map
    QCN Quake Catcher Network map

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  • richardmitnick 9:48 am on December 5, 2016 Permalink | Reply
    Tags: , , Breakthrough Prizes, , Roeland Nusse, , , Wnt signaling proteins   

    From Stanford: “Roeland Nusse wins $3 million Breakthrough Prize” 

    Stanford University Name
    Stanford University

    12.4.16
    Krista Conger

    1
    Roeland Nusse was awarded the 2017 Breakthrough Prize in life sciences for his contributions to the understanding a signaling molecule called Wnt. Norbert von der Groeben

    The developmental biologist was honored for helping to decode how Wnt signaling proteins affect embryonic development, cancer and the activity of tissue-specific adult stem cells that repair damage after injury or disease.

    Roeland Nusse, PhD, the Virginia and Daniel K. Ludwig Professor in Cancer Research and a Howard Hughes Medical Institute investigator, was honored this evenng with a 2017 Breakthrough Prize in life sciences.

    Nusse was awarded the $3 million prize for his contributions to the understanding of how a signaling molecule called Wnt affects normal development, cancer and the functions of adult stem cells in many tissues throughout the body.

    “This is a complete surprise,” said Nusse, who is professor and chair of developmental biology. “My gratitude goes out to many people — my past and present postdoctoral scholars and graduate students and my former mentors have all contributed to the success of my research. The research and collaborative environment at Stanford and the long-term support from the Howard Hughes Medical Institute have also been fantastic. I see this award as a great honor for the entire community.”

    The Breakthrough Prizes, initiated in 2013, honor paradigm-shifting research and discovery in the fields of life sciences, fundamental physics and mathematics. In total, about $25 million was awarded at this year’s ceremony, a black-tie, red-carpet affair at the NASA Ames Research Center in Mountain View. The event was hosted by actor Morgan Freeman. The Grammy Award-winning pop star Alicia Keys provided entertainment.

    “Roel’s pioneering work has provided deep insights into an essential molecular signaling pathway that controls normal embryonic development and adult tissue repair, and that contributes to cancer when it is not properly regulated. His work has served as a model for many others in our field and accelerated further studies of these critical processes,” said Stanford President Marc Tessier-Lavigne, PhD. “We are grateful that the Breakthrough Prize recognizes the work of scientific leaders who are inspiring others to pursue discovery that is truly transformative, benefiting all of humanity.”

    Nusse’s interest in Wnt began in the 1980s as a postdoctoral scholar in the laboratory of Harold Varmus, MD, who was then on the faculty of UC-San Francisco. In 1982, Nusse discovered the Wnt1 gene, which was abnormally activated in a mouse model of breast cancer. He subsequently discovered that members of the Wnt family of proteins also play critical roles in embryonic development, cell differentiation and tissue regeneration.

    “Roel has devoted his career to identifying one of the major signaling molecules in embryonic development, and clarifying its role in cancer development and in tissue regeneration,” said Lloyd Minor, MD, dean of the School of Medicine. “The importance of Wnt signaling in these processes cannot be overestimated. His work has been the foundation of much of modern developmental biology, and we are very proud of his contributions.”

    Nusse’s more recent work has focused on understanding how Wnt family members control the function of adult stem cells in response to injury or disease. In 1996, he identified the cell-surface receptor to which Wnt proteins bind to control cells’ functions, and in 2002 he was the first to purify Wnt proteins — an essential step to understanding how they work at a molecular level.

    “My work has shifted significantly over the years due to the influence of my Stanford colleagues, although it has always been focused on Wnt,” said Nusse. “When I arrived at Stanford, I was studying the involvement of the Wnt proteins in mouse development and cancer. I then switched to fruit flies, and then to the study of adult stem cells. Stanford has supported me during this evolution of my research career.”

    Nusse’s lab is currently devoted to understanding how Wnt signaling affects the function of adult stem cells in the liver to help the organ heal after injury, as well as what role Wnt signaling might play in the development of liver cancer.

    “The Breakthrough Prizes are a sign of the times,” said Nusse. “Together with the recently announced Chan Zuckerberg Initiative, they show how the wealth of Silicon Valley is now making an impact not just in the field of computer science, but also in biomedical fields. This is very exciting.”

    Nusse is a member of the Ludwig Center for Cancer Stem Cell Research and Medicine at Stanford, of the Stanford Cancer Institute and of the Stanford Institute for Stem Cell Biology and Regenerative Medicine. He was awarded the Peter Debye Prize from the University of Maastricht in 2000. He is a member of the U.S. National Academy of Sciences, the European Molecular Biology Organization and the Royal Dutch Academy of Sciences. He is also a fellow of the American Academy of Arts and Sciences.

    In all, seven $3 million Breakthrough Prizes — five in the life sciences, one in fundamental physics and one in mathematics — were awarded to 12 recipients. In addition, a special Breakthrough Prize in fundamental physics was awarded to the more than one thousand researchers who proved the existence of gravitational waves in February of 2016.

    Probing for dark matter

    2
    Peter Graham. No image credit

    In addition, three $100,000 New Horizons in Physics Prizes were awarded at the ceremony. Peter Graham, PhD, an assistant professor of physics at Stanford, shared one of them with Asimina Arvanitaki of the Perimeter Institute in Ontario, Canada, and Surjeet Rajendran of the University of California-Berkeley, for “pioneering a wide range of new experimental probes of fundamental physics.”

    Graham earned a PhD at Stanford and completed postdoctoral studies at the Stanford Institute for Theoretical Physics before joining the Stanford faculty in 2010. In 2014, he received an Early Career Award from the Department of Energy.

    Graham has developed new experiments to detect particles known as dark matter, which physicists have reason to believe exist but haven’t yet been able to detect. Physicists have theorized about what dark matter might be, and based on that work have designed experiments to detect those theorized particles. However, those experiments would miss one possible variant of what dark matter might be, known as an axion.

    “It was a scary scenario that this might be what dark matter is and our current experiments wouldn’t detect it,” Graham said.

    Graham designed new experimental approaches that would detect axions if they turn out to be what make up dark matter. “This prize is a huge honor,” Graham said. “It’s great to get recognition from the community for this new direction; it will really help this emerging field.”

    Three $100,000 New Horizons in Mathematics prizes were also awarded at the Breakthrough Prize ceremony.

    In addition, two teenagers — one from Peru and one from Singapore — each won the 2017 Breakthrough Junior Challenge. They will each receive $400,000 in educational prizes.

    The Breakthrough Prizes are funded by grants from the Brin Wojcicki Foundation, established by Google founder Sergey Brin and 23andMe founder Anne Wojcicki; Mark Zuckerberg’s fund at the Silicon Valley Community Foundation; Alibaba founder Jack Ma’s foundation; and DST Global founder Yuri Milner’s foundation. Recipients are chosen by committees comprised of prior prizewinners.

    Amy Adams, director for science communications at the Stanford News Service, contributed to this article.

    See the full article here .

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    Leland and Jane Stanford founded the University to “promote the public welfare by exercising an influence on behalf of humanity and civilization.” Stanford opened its doors in 1891, and more than a century later, it remains dedicated to finding solutions to the great challenges of the day and to preparing our students for leadership in today’s complex world. Stanford, is an American private research university located in Stanford, California on an 8,180-acre (3,310 ha) campus near Palo Alto. Since 1952, more than 54 Stanford faculty, staff, and alumni have won the Nobel Prize, including 19 current faculty members

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  • richardmitnick 9:33 am on December 5, 2016 Permalink | Reply
    Tags: , ALMA measures size of planets’ seeds, , , HD 142527, , , Radio-wave polarization   

    From ALMA: “ALMA measures size of planets’ seeds” 

    ESO/NRAO/NAOJ ALMA Array
    ESO/NRAO/NAOJ ALMA Array in Chile in the Atacama at Chajnantor plateau, at 5,000 metres
    ALMA

    05 December 2016
    Nicolás Lira T.
    Education and Public Outreach Coordinator
    Joint ALMA Observatory
    Santiago, Chile
    Tel: +56 2 24 67 65 19
    Cell: +56 9 94 45 77 26
    Email: nicolas.lira@alma.cl

    Masaaki Hiramatsu
    Education and Public Outreach Officer, NAOJ Chile
    Observatory Tokyo, Japan
    Tel: +81 422 34 3630
    E-mail: hiramatsu.masaaki@nao.ac.jp

    Richard Hook
    Public Information Officer, ESO
    Garching bei München, Germany
    Tel: +49 89 3200 6655
    Cell: +49 151 1537 3591
    Email: rhook@eso.org

    Charles E. Blue
    Public Information Officer
    National Radio Astronomy Observatory
    Charlottesville, Virginia, USA
    Tel: +1 434 296 0314
    Cell: +1 202 236 6324
    E-mail: cblue@nrao.edu

    1
    Dust disk around the young star HD 142527 observed with ALMA. Credit: ALMA (ESO/NAOJ/NRAO), Kataoka et al.

    Researchers using the Atacama Large Millimeter/submillimeter Array (ALMA), have for the first time, achieved a precise size measurement of small dust particles around a young star through radio-wave polarization. ALMA’s high sensitivity for detecting polarized radio waves made possible this important step in tracing the formation of planets around young stars.

    Astronomers have believed that planets are formed from gas and dust particles, although the details of the process have been veiled. One of the major enigmas is how dust particles as small as 1 micrometer aggregate to form a rocky planet with a diameter of 10 thousand kilometers. Difficulty in measuring the size of dust particles has prevented astronomers from tracing the process of dust growth.

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    Artist’s impression of a dust ring around the young star HD 142527. Dust around the star has an asymmetric distribution. Credit: NAOJ

    Akimasa Kataoka, a Humboldt Research Fellow stationed at Heidelberg University and the National Astronomical Observatory of Japan (NAOJ), tackled this problem. He and his collaborators have theoretically predicted that, around a young star, radio waves scattered by the dust particles should carry unique polarization features. He also noticed that the intensity of polarized emissions allows us to estimate the size of dust particles far better than other methods.

    To test their prediction, the team led by Kataoka observed the young star HD 142527 with ALMA [1] and discovered, for the first time, the unique polarization pattern in the dust disk around the star. As predicted, the polarization has a radial direction in most parts of the disk, but at the edge of the disk, the direction is flipped perpendicular to the radial direction.

    Comparing the observed intensity of the polarized emissions with the theoretical prediction, they determined that the size of the dust particles is at most 150 micrometers. This is the first estimation of the dust size based on polarization. Surprisingly, this estimated size is more than 10 times smaller than previously thought.

    “In the previous studies, astronomers have estimated the size based on radio emissions assuming hypothetical spherical dust particles,” explains Kataoka. “In our study, we observed the scattered radio waves through polarization, which carries independent information from the thermal dust emission. Such a big difference in the estimated size of dust particles implies that the previous assumption might be wrong.”

    3
    Polarization pattern obtained by ALMA around the young star HD 142527. Contours show the total intensity of dust emissions and the color image shows the intensity of polarized emissions. White bars show the direction of polarization. Credit: ALMA (ESO/NAOJ/NRAO), Kataoka et al.

    The team’s idea to solve this inconsistency is to consider fluffy, complex-shaped dust particles, not simple spherical dust [2] . In the macroscopic view, such particles are indeed large, but in the microscopic view, each small part of a large dust particle scatters radio waves and produces unique polarization features. Per the present study, astronomers obtain these “microscopic” features through polarization observations. This idea might prompt astronomers to reconsider the previous interpretation of observational data.

    “The polarization fraction of radio waves from the dust disk around HD 142527 is only a few percent. Thanks to ALMA’s high sensitivity, we have detected such a tiny signal to derive information about the size and shape of the dust particles,” said Kataoka. “This is the very first step in the research on dust evolution with polarimetry, and I believe the future progress will be full of excitement.”

    Notes

    [1]. HD 142527 is located 500 light-years away from the Earth, in the direction of the constellation Lupus, the Wolf. The age of the star is estimated to be 5 million years old and its mass twice that of the Sun. HD 142527 is a popular target among astronomers to study planet formation and several findings about it have previously been reported from ALMA (for example, “ALMA Discovers a Formation Site of a Giant Planetary System”) and the Subaru Telescope (for example, “Diversity the Norm in Protoplanetary Disks: Astronomers Find Donuts, Spirals and Now Banana Splits”).

    [2]. Prior to the ALMA observations, Kataoka had propounded fluffy dust particles around young stars. Such particles are not only favored to explain ALMA’s observational results, but also help overcome other big problems in the dust aggregation process. For details, see the press release “The seeds of planets are fluffy” issued in 2013.

    Additional information

    These observation results were published as Kataoka et al. Millimeter Polarization Observation of the Protoplanetary Disk around HD 142527 in the Astrophysical Journal Letters in November 2016.

    The research team members are:

    Akimasa Kataoka (Humboldt Research Fellowship for Postdoctoral Researchers / Heidelberg University / National Astronomical Observatory of Japan / former Postdoctral Fellowship for Research Abroad at Japan Society for Promoting Science), Takashi Tsukagoshi (Ibaraki University), Munetake Momose (Ibaraki University), Hiroshi Nagai (National Astronomical Observatory of Japan), Takayuki Muto (Kogakuin University), Cornelis P. Dullemond (Heidelberg University), Adriana Pohl (Heidelberg University / Max Planck Institute for Astronomy), Misato Fukagawa (Nagoya University), Hiroshi Shibai (Osaka University), Tomoyuki Hanawa (Chiba University), Koji Murakawa (Osaka Sangyo University)

    This research was supported by a Grant-in-Aid from the Japan Society for the Promotion of Science and the Ministry of Education, Culture, Sports, Science and Technology, Japan (No. 23103004、15K17606、26800106).

    See the full article here .

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    The Atacama Large Millimeter/submillimeter Array (ALMA), an international astronomy facility, is a partnership of Europe, North America and East Asia in cooperation with the Republic of Chile. ALMA is funded in Europe by the European Organization for Astronomical Research in the Southern Hemisphere (ESO), in North America by the U.S. National Science Foundation (NSF) in cooperation with the National Research Council of Canada (NRC) and the National Science Council of Taiwan (NSC) and in East Asia by the National Institutes of Natural Sciences (NINS) of Japan in cooperation with the Academia Sinica (AS) in Taiwan.

    ALMA construction and operations are led on behalf of Europe by ESO, on behalf of North America by the National Radio Astronomy Observatory (NRAO), which is managed by Associated Universities, Inc. (AUI) and on behalf of East Asia by the National Astronomical Observatory of Japan (NAOJ). The Joint ALMA Observatory (JAO) provides the unified leadership and management of the construction, commissioning and operation of ALMA.

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  • richardmitnick 2:28 pm on December 4, 2016 Permalink | Reply
    Tags: , , Cold brown dwarfs, ,   

    From Science: “Alien life could thrive in the clouds of failed stars” 

    ScienceMag
    Science Magazine

    1
    The comfortably warm atmosphere of a brown dwarf is an underappreciated potential home for alien life, scientists say. Mark Garlick/Science Source

    Dec. 2, 2016
    Joshua Sokol

    There’s an abundant new swath of cosmic real estate that life could call home—and the views would be spectacular. Floating out by themselves in the Milky Way galaxy are perhaps a billion cold brown dwarfs, objects many times as massive as Jupiter but not big enough to ignite as a star. According to a new study, layers of their upper atmospheres sit at temperatures and pressures resembling those on Earth, and could host microbes that surf on thermal updrafts.

    The idea expands the concept of a habitable zone to include a vast population of worlds that had previously gone unconsidered. “You don’t necessarily need to have a terrestrial planet with a surface,” says Jack Yates, a planetary scientist at the University of Edinburgh in the United Kingdom, who led the study.

    Atmospheric life isn’t just for the birds. For decades, biologists have known about microbes that drift in the winds high above Earth’s surface. And in 1976, Carl Sagan envisioned the kind of ecosystem that could evolve in the upper layers of Jupiter, fueled by sunlight. You could have sky plankton: small organisms he called “sinkers.” Other organisms could be balloonlike “floaters,” which would rise and fall in the atmosphere by manipulating their body pressure. In the years since, astronomers have also considered the prospects of microbes in the carbon dioxide atmosphere above Venus’s inhospitable surface.

    Yates and his colleagues applied the same thinking to a kind of world Sagan didn’t know about. Discovered in 2011, some cold brown dwarfs have surfaces roughly at room temperature or below; lower layers would be downright comfortable. In March 2013, astronomers discovered WISE 0855-0714, a brown dwarf only 7 light-years away that seems to have water clouds in its atmosphere. Yates and his colleagues set out to update Sagan’s calculations and to identify the sizes, densities, and life strategies of microbes that could manage to stay aloft in the habitable region of an enormous atmosphere of predominantly hydrogen gas. Sink too low and you are cooked or crushed. Rise too high and you might freeze.

    On such a world, small sinkers like the microbes in Earth’s atmosphere or even smaller would have a better chance than Sagan’s floaters, the researchers will report in an upcoming issue of The Astrophysical Journal. But a lot depends on the weather: If upwelling winds are powerful on free-floating brown dwarfs, as seems to be true in the bands of gas giants like Jupiter and Saturn, heavier creatures can carve out a niche. In the absence of sunlight, they could feed on chemical nutrients. Observations of cold brown dwarf atmospheres reveal most of the ingredients Earth life depends on: carbon, hydrogen, nitrogen, and oxygen, though perhaps not phosphorous.

    The idea is speculative but worth considering, says Duncan Forgan, an astrobiologist at the University of St. Andrews in the United Kingdom, who did not participate in the study but says he is close to the team. “It really opens up the field in terms of the number of objects that we might then think, well, these are habitable regions.”

    So far, only a few dozen cold brown dwarfs have been discovered, though statistics suggest there should be about 10 within 30 light-years of Earth. These should be ripe targets for the James Webb Space Telescope (JWST), which is sensitive in the infrared where brown dwarfs shine brightest.

    NASA/ESA/CSA Webb Telescope annotated
    NASA/ESA/CSA Webb Telescope annotated

    After it launches in 2018, the JWST should reveal the weather and the composition of their atmospheres, says Jackie Faherty, an astronomer at the Carnegie Institution for Science in Washington, D.C. “We’re going to start getting gorgeous spectra of these objects,” she says. “This is making me think about it.”

    Testing for life would require anticipating a strong spectral signature of microbe byproducts like methane or oxygen, and then differentiating it from other processes, Faherty says. Another issue would be explaining how life could arise in an environment that lacks the water-rock interfaces, like hydrothermal vents, where life is thought to have begun on Earth. Perhaps life could develop through chemical reactions on the surfaces of dust grains in the brown dwarf’s atmosphere, or perhaps it gained a foothold after arriving as a hitchhiker on an asteroid. “Having little microbes that float in and out of a brown dwarf atmosphere is great,” Forgan says. “But you’ve got to get them there first.”

    See the full article here .

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