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  • richardmitnick 1:42 pm on August 31, 2016 Permalink | Reply
    Tags: , , Medicine, , Unravel bipolar disorder and schizophrenia   

    From Salk: “Johns Hopkins and Salk co-lead $15 million initiative to unravel bipolar disorder and schizophrenia” 

    Salk Institute bloc

    Salk Institute for Biological Studies

    August 31, 2016
    No writer credit found

    Partnership of government, academics and industry will develop new ways of studying and screening drugs for major psychiatric illnesses.

    The Johns Hopkins University School of Medicine and the Salk Institute for Biological Studies will co-lead a $15.4 million effort to develop new systems for quickly screening libraries of drugs for potential effectiveness against schizophrenia and bipolar disorder, the National Institute of Mental Health (NIMH) has announced. The consortium, which includes four academic or nonprofit institutions and two industry partners, will be led by Hongjun Song, PhD, of Johns Hopkins and Rusty Gage, PhD, of Salk.

    Bipolar disorder affects more than 5 million Americans, and treatments often help only the depressive swings or the opposing manic swings, not both. And though schizophrenia is a devastating disease that affects about 3 million Americans and many more worldwide, scientists still know very little about its underlying causes—which cells in the brain are affected and how—and existing treatments target symptoms only.

    With the recent advance of induced pluripotent stem cell (iPSC) technology, researchers are able to use donated cells, such as skin cells, from a patient and convert them into any other cell type, such as neurons. Generating human neurons in a dish that are genetically similar to patients offers researchers a potent tool for studying these diseases and developing much-needed new therapies.

    A major aim of this collaboration is to improve the quality of iPSC technology, which has been limited in the past by a lack of standards in the field and inconsistent practices among different laboratories. “There has been a bottleneck in stem cell research,” says Song, a professor of neurology and neuroscience at Johns Hopkins. “Every lab uses different protocols and cells from different patients, so it’s really hard to compare results. This collaboration gathers the resources needed to create robust, reproducible tests that can be used to develop new drugs for mental health disorders.”

    “IPSCs are a powerful platform for studying the underlying mechanisms of disease,” says Gage, a professor of genetics at Salk. “Collaborations that bring together academic and industry partners, such as this one enabled by NIMH, will greatly facilitate the improvement of iPSC approaches for high-throughput diagnostic and drug discovery.”

    The teams will use iPSCs generated from more than 50 patients with schizophrenia or bipolar disorder so that a wide range of genetic differences is taken into account. By coaxing iPSCs to become four different types of brain cells, the teams will be able to see which types are most affected by specific genetic differences and when those effects may occur during development.

    First the researchers must figure out, at the cellular level, what features characterize a given illness in a given brain cell type. To do that, they will assess the cells’ shapes, connections, energy use, division and other properties. They will then develop a way of measuring those characteristics that works on a large scale, such as recording the activity of cells under hundreds of different conditions simultaneously.

    Once a reliable, scalable and reproducible test system has been developed, the industry partners will have the opportunity to use it to identify or develop drugs that might combat mental illness. “This exciting new research has great potential to expedite drug discovery by using human cells from individuals who suffer from these devastating illnesses. Starting with a deeper understanding of each disorder should enable the biopharmaceutical industry to design drug discovery strategies that are focused on molecular pathology,” says Husseini K. Manji, M.D., F.R.C.P.C., global therapeutic area head of neuroscience for Janssen Research & Development.

    The researchers also expect to develop a large body of data that will shed light on the molecular and genetic differences between bipolar disorder and schizophrenia. And, since other mental health disorders share some of the genetic variations found in schizophrenia and bipolar disorder, the data will likely inform the study of many illnesses.

    The National Cooperative Reprogrammed Cell Research Groups program, which is funding the research, was introduced by the National Institute of Mental Health in 2013 to overcome barriers to collaboration by creating precompetitive agreements that harness the unique strengths of academic and industry research. The federal-academic-industry collaboration will bring together leading experts in the fields of stem cells and neuropsychiatric disorders:

    Academic Partners:

    Hongjun Song, Professor, the Johns Hopkins University School of Medicine
    Rusty Gage, Professor, Laboratory of Genetics at the Salk Institute
    Sue O’Shea, Director, Michigan Pluripotent Stem Cell Core and Professor, University of Michigan
    Anne Bang, Director, Conrad Prebys Center for Chemical Genomics at the Sanford Burnham Prebys Medical Discovery Institute

    Industry Partners:

    Guang Chen, Janssen fellow, Scientific Director of Neuroscience, Janssen Research & Development
    Jeffrey S. Nye, Vice President, Neuroscience Innovation and Partnership Strategy, Janssen Research & Development, J&J Innovation
    Husseini K. Manji, Global Therapeutic Area Head of Neuroscience, Janssen Research & Development
    Paul Doran, Strategic Alliance Manager, Cellular Dynamics International

    Funding Announcement: http://grants.nih.gov/grants/guide/pa-files/PAR-13-225.html
    Supported by NIMH Cooperative Agreement Number U19MH106434

    See the full article here .

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    Salk Institute Campus

    Every cure has a starting point. Like Dr. Jonas Salk when he conquered polio, Salk scientists are dedicated to innovative biological research. Exploring the molecular basis of diseases makes curing them more likely. In an outstanding and unique environment we gather the foremost scientific minds in the world and give them the freedom to work collaboratively and think creatively. For over 50 years this wide-ranging scientific inquiry has yielded life-changing discoveries impacting human health. We are home to Nobel Laureates and members of the National Academy of Sciences who train and mentor the next generation of international scientists. We lead biological research. We prize discovery. Salk is where cures begin.

  • richardmitnick 9:08 am on August 31, 2016 Permalink | Reply
    Tags: Medicine, Motor neuron disease, Sarah Rea, UWA,   

    From UWA: Women in STEM – “Searching for a cure” Sarah Rea 


    University of Western Australia

    Sarah Rea, NHMRC-ARC Dementia Research Fellow

    Meeting a boy with cerebral palsy set molecular biologist Sarah Rea on her career path to finding a cure for motor neuron disease.

    “I left high school without finishing Year 11, so I needed to do my high school education as a mature age student,” Sarah says.

    “I initially wanted to study speech pathology to help kids like him, however I realised speech pathology was not likely to help children like him overly much. I chose to study Molecular Biology and Biomedical Science instead, because I became fascinated by genetics and wanted to learn more so I could help try to cure diseases.”

    Sarah now focuses on how specific genetic changes cause motor neuron disease (MND) and frontotemporal dementia (FTD).

    “I became aware of an overlap between MND and FTD genetic factors with those of another disease that my work focuses on – Paget’s disease of bone,” Sarah says.

    While completing her PhD with UWA, Sarah was mentored and encouraged through a UWA Collaboration Award and was given the opportunity to travel and present her research in various forums, all the while having two children.

    “I think the hardest thing for me was finding a life balance where I wasn’t able to be a perfect mother or a perfect researcher,” Sarah says.

    “Being a scientist and having a high-stress career has allowed for a huge amount of personal growth. You never know what you are capable of until you push yourself to the limits.

    “My aim is to find a cure for motor neuron disease. I am realistic that this is perhaps an ‘impossible’ goal, but I believe it is one worth pursuing.”

    See the full article here .

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  • richardmitnick 7:11 am on August 31, 2016 Permalink | Reply
    Tags: , , , Medicine, Study Finds Potential New Biomarker for Cancer Patient Prognosis   

    From LBNL: “Study Finds Potential New Biomarker for Cancer Patient Prognosis” 

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    Berkeley Lab

    August 31, 2016
    Sarah Yang
    (510) 486-4575

    To treat or not to treat? That is the question researchers at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) hope to answer with a new advance that could help doctors and their cancer patients decide if a particular therapy would be worth pursuing.

    The centromeres and kinetochores of a chromosome play critical roles during cell division. In mitosis, microtubule spindle fibers attach to the kinetochores, pulling the chromatids apart. A breakdown in this process causes chromosome instability. Researchers have linked the overexpression of centromere and kinetochore genes to cancer patient outcome after adjuvant therapies. (Credit: Zosia Rostomian/Berkeley Lab)

    Berkeley Lab researchers identified 14 genes regulating genome integrity that were consistently overexpressed in a wide variety of cancers. They then created a scoring system based upon the degree of gene overexpression. For several major types of cancer, including breast and lung cancers, the higher the score, the worse the prognosis. Perhaps more importantly, scores could accurately predict patient response to specific cancer treatments.

    The researchers said the findings, published today in the journal Nature Communications, could lead to a new biomarker for the early stages of tumor development. The information obtained could help reduce the use of cancer treatments that have a low probability of helping.

    Overtreating Cancer

    “The history of cancer treatment is filled with overreaction,” said the study’s principal investigator, Gary Karpen, a senior scientist in Berkeley Lab’s Division of Biological Systems and Engineering with a joint appointment at UC Berkeley’s Department of Molecular and Cell Biology. “It is part of the ethics of cancer treatment to err on the side of overtreatment, but these treatments have serious side effects associated with them. For some people, it may be causing more trouble than if the growth was left untreated.”

    One of the challenges is that there has been no reliable way to determine at an early stage if patients will respond to chemotherapy and radiation therapy, said study lead author Weiguo Zhang, a project scientist at Berkeley Lab.

    “Even for early stage cancer patients, such as lung cancers, adjuvant chemotherapy and radiotherapy are routinely used in treatment, but overtreatment is a major challenge,” said Zhang. “For certain types of early stage lung cancer patients, there are estimates that adjuvant chemotherapy improves five-year survival only about 10 percent, on average, which is not great considering the collateral damage caused by this treatment.”

    The researchers noted that there are many factors a doctor and patient must consider in treatment decisions, but this biomarker could become a valuable tool when deciding whether to use a particular therapy or not.

    Study co-author Anshu Jain, an oncologist at the Ashland Bellefonte Cancer Center in Kentucky and a clinical instructor at the Yale School of Medicine, added that the real value of this work may be in helping doctors and patients consider alternatives to the typical course of treatment.

    “These findings are very exciting,” said Jain. “The biomarker score provides predictive and prognostic information separate from and independent of clinical and pathologic tumor characteristics that oncologists have available today and which often provide only limited clinical value.”

    Hunting for new biomarkers

    The study authors focused on genes regulating the function of centromeres and kinetochores – the essential sites on chromosomes that spindle fibers attach to during cell division – based upon results from earlier research by the Karpen group and other labs in the field. In normal cell division, microtubule spindles latch on to the kinetochores, pulling the chromosome’s two chromatids apart.

    What the Karpen team previously found in fruit flies is that the overexpression of a specific centromere protein resulted in extra spindle attachment sites on the chromosomes.

    “This essentially makes new centromeres functional at more than one place on the chromosome, and this is a huge problem because the spindle tries to connect to all the sites,” said Karpen. “If you have two or more of these sites on the chromosome, the spindles are pulling in too many directions, and you end up breaking the chromosome during cell division. So overexpression of these genes may be a major contributing factor to chromosomal instability, which is a hallmark of all cancers.”

    This chromosomal instability has long been recognized as a characteristic of cancer, but its cause has remained unclear.

    To determine if centromeres play a role in chromosome instability in human cancers, the researchers analyzed many public datasets from the National Center for Biotechnology Information, the Broad Institute and other organizations that together contained thousands of human clinical tumor samples from at least a dozen types of cancers. The researchers screened 31 genes involved in regulating centromere and kinetochore function to find the 14 that were consistently overexpressed in cancer tissue.

    The extensive records included information on DNA mutations and chromosome rearrangements, the presence and levels of specific proteins, the stage of tumor growth at the time the patient was diagnosed, treatments given, and patient status in the years following diagnosis and treatment. This allowed the researchers to correlate the centromere and kinetochore gene expression score (CES) with patient outcomes either with or without treatments.

    Genome Instability and Cancer Therapy

    “We were surprised to find such a strong correlation between CES and things like whether the patient survived five years later,” said Karpen. “Another finding – one that is counterintuitive – is that high expression of these centromere genes is also related to more effective chemotherapy and radiation therapy.”

    The researchers hypothesized that the degree of chromosomal instability may also make cancer cells more vulnerable to the effects of chemotherapy or radiation therapy.

    “In other words, there’s a threshold of genome instability,” said Zhang. “At low to medium-high levels, the cancer thrives. But at much higher levels, the cancer cells are more susceptible to the additional DNA damage caused by the treatment. This is a really key point.”

    The researchers pointed out that they found no link between very high levels of genome instability and improved patient survival without adjuvant treatments.

    Translating these findings into clinical advice and practice will take more research, the study authors caution. They are working to find that threshold of genome instability so that in the future, doctors and patients can make informed decisions about how to move forward.

    “Future steps will include investigating the CES in prospective clinical studies for validation in carefully selected patient cohorts,” said Jain. “By establishing the clinical significance of the CES, oncologists will have greater confidence in guiding cancer patients toward treatments with the greatest benefit.”

    Other co-authors of the study are Jian-Hua Mao at Berkeley Lab’s Division of Biological Systems and Engineering; Wei Zhu at the Cellular Biomedicine Group in Shanghai; and Ke Liu and James Brown at Berkeley Lab’s Division of Environmental Genomics and Systems Biology. Mao and Zhu provided critical expertise in bioinformatics for this research.

    The National Institutes of Health supported this work.

    See the full article here .

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  • richardmitnick 6:49 am on August 30, 2016 Permalink | Reply
    Tags: , Medicine, , Parkinson’s disease   

    From U Cambridge: “Tiny changes in Parkinson’s protein can have “dramatic” impact on processes that lead to the disease” 

    U Cambridge bloc

    Cambridge University

    30 Aug 2016
    Tom Kirk

    Image of “amyloid fibrils”; thread-like structures which form after the protein alpha-synuclein aggregates. Plaques (protein deposits) consisting of this protein have been found in the brains of Parkinson ’s Disease patients and linked to disease. Credit: Patrick Flagmeier

    In a new study, a team of academics at the Centre for Misfolding Diseases, in the Department of Chemistry at the University of Cambridge, show that tiny changes in the amino acid sequence of the protein alpha-synuclein can have a dramatic effect on microscopic processes leading to its aggregation that may occur in the brain, eventually resulting in someone being diagnosed with Parkinson’s Disease.

    Alpha-synuclein is a protein made up of 140 amino acids, and under normal circumstances plays an important part in helping with the smooth flow of chemical signals in the brain.

    Parkinson’s Disease is thought to arise because, for reasons researchers still do not fully understand, the same protein sometimes malfunctions. Instead of adopting the specific structural form needed to do its job, it misfolds and begins to cluster, creating toxic, thread-like structures known as amyloid fibrils. In the case of Parkinson’s Disease, these protein deposits are referred to as Lewy-bodies.

    The new study examined mutated forms of alpha-synuclein which have been found in people from families with a history of Parkinson’s Disease. In all cases, these mutations involved just one change to the protein’s amino acid sequence.

    Although the differences in the sequence are small, the researchers found that they can have a profound effect on how quickly or slowly fibrils start to form. They also found that the mutations strongly influence a process called “secondary nucleation”, in which new fibrils are formed, in an auto-catalytic manner, at the surface of existing ones and thus enable the disease to spread.

    The study stresses that these findings do not explain why humans get the disease. Parkinson’s Disease does not always emerge as a result of the mutations and has multiple, complex causes, which are not fully understood.

    Patrick Flagmeier, a PhD student at St John’s College, University of Cambridge, and the study’s lead author, said: “As a finding, it helps us to understand fundamental things about the system by which this disease emerges. In the end, if we can understand all of this better, that can help us to develop therapeutic strategies to confront it. Our hope is that this study will contribute to the global effort towards comprehending why people with these mutations get the disease more frequently, or at a younger age.”

    Although people who do not have mutated forms of alpha-synuclein can still develop Parkinson’s Disease, the five mutations studied by the research team were already known as “familial” variants – meaning that they recur in families where the disease has emerged, and seem to increase the likelihood of its onset.

    What was not clear, until now, is why they have this effect. “We wanted to know how these specific changes in the protein’s sequence influence its behaviour as it aggregates into fibrils,” Flagmeier said.

    To understand this, the researchers conducted lab tests in which they added each of the five mutated forms of alpha-synuclein, as well as a standard version of the protein, to samples simulating the initiation of fibril formation, their growth and their proliferation.

    The first round of tests examined the initiation of aggregation, using artificial samples recreating conditions in which misfolded alpha-synuclein attaches itself to small structures that are present inside brain cells called lipid vesicles, and then begins to cluster.

    The researchers then tested how the different versions of the protein influence the ability of pre-formed fibrils to extend and grow. Finally, they tested the impact of mutated proteins on secondary nucleation, in which, under specific conditions, the fibrils can multiply and start to spread.

    Overall, the tests revealed that while the mutated forms of alpha-synuclein do not notably influence the fibril growth, they do have a dramatic effect on both the initial formation of the fibrils, and their secondary nucleation. Some of the mutated forms of the protein made these processes considerably faster, while others made it almost “undetectably slow”, according to the researchers’ report.

    “We have only recently discovered the autocatalytic amplification process of alpha-synuclein fibrils, and the results of the present study will help us to understand in much more detail the mechanism behind this process, and in what ways it differs from the initial formation of aggregates.” said Dr. Alexander Buell, one of the senior authors on the study.

    Why the mutations have this impact remains unclear, but the study opens the door to understanding this in detail by identifying, for the first time, that they have such a dramatic impact on very particular stages of the process.

    Dr. Céline Galvagnion, another of the senior authors on the study, said: “This study quantitatively correlates individual changes in the amino acid sequence of alpha-synuclein with its tendency to aggregate. However, the effect of these mutations on other parameters such as the loss of the protein’s function and the efficiency of clearance of alpha-synuclein needs to be taken into account to fully understand the link between the familial mutations of alpha-synuclein and the onset of Parkinson’s Disease.”

    “The effects we observed were changes of several orders of magnitude and it was unexpected to observe such dramatic effects from single-point mutations,” Flagmeier said. “It seems that these single-point mutations in the sequence of alpha-synuclein play an important role in influencing particular microscopic steps in the aggregation process that may lead to Parkinson’s Disease.”

    The full study, which also involves Professors Chris Dobson and Tuomas Knowles, is published in the journal, Proceedings of the National Academy of Sciences.


    Flagmeier, P. et. al: Mutations associated with familial Parkinson’s disease alter the initiation and amplification steps of α-synuclein aggregation. PNAS (2016): DOI: 10.1073/pnas.1604645113

    See the full article here .

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    The University of Cambridge (abbreviated as Cantab in post-nominal letters) is a collegiate public research university in Cambridge, England. Founded in 1209, Cambridge is the second-oldest university in the English-speaking world and the world’s fourth-oldest surviving university. It grew out of an association of scholars who left the University of Oxford after a dispute with townsfolk. The two ancient universities share many common features and are often jointly referred to as “Oxbridge”.

    Cambridge is formed from a variety of institutions which include 31 constituent colleges and over 100 academic departments organised into six schools. The university occupies buildings throughout the town, many of which are of historical importance. The colleges are self-governing institutions founded as integral parts of the university. In the year ended 31 July 2014, the university had a total income of £1.51 billion, of which £371 million was from research grants and contracts. The central university and colleges have a combined endowment of around £4.9 billion, the largest of any university outside the United States. Cambridge is a member of many associations and forms part of the “golden triangle” of leading English universities and Cambridge University Health Partners, an academic health science centre. The university is closely linked with the development of the high-tech business cluster known as “Silicon Fen”.

  • richardmitnick 5:55 am on August 30, 2016 Permalink | Reply
    Tags: , Medicine,   

    From UCLA: “UCLA researchers develop method to speed up detection of infectious diseases, cancer” 

    UCLA bloc


    August 26, 2016
    Matthew Chin

    UCLA researchers were able to use a molecular chain reaction to detect the presence of proteins in blood and plasma in a way that is faster and simpler.

    A team of UCLA researchers has found a way to speed and simplify the detection of proteins in blood and plasma opening up the potential for diagnosing the early presence of infectious diseases or cancer during a doctor’s office visit. The new test takes about 10 minutes as opposed to two to four hours for current state-of-the-art tests.

    The new approach overcame several key challenges in detecting proteins that are biomarkers of disease. First, these proteins are often at low abundance in body fluids and accurately identifying them requires amplification processes. The current approach uses enzymes to amplify the signal from proteins. However, enzymes can break down if they are not stored at proper temperatures. Also, to avoid a false positive, excess enzymes need to be washed away. This increases the complexity and cost of the test.

    The study, which included researchers from the Henry Samueli School of Engineering and Applied Science, the California NanoSystems Institute, and the David Geffen School of Medicine, was published online in the journal ACS Nano.

    The researchers included lead author Donghyuk Kim, a UCLA post-doctoral researcher in bioengineering and Dino Di Carlo, professor of bioengineering. They collaborated with Aydogan Ozcan, Chancellor’s Professor of Electrical Engineering and Bioengineering and Omai Garner, assistant professor of pathology and medicine at the David Geffen School of Medicine at UCLA.

    The UCLA team devised an approach to amplify a protein signal without any enzymes, thus eliminating the need for a complex system to wash away excess enzymes, and that would work only in the presence of the target protein. This new approach made use of a molecular chain reaction that was strongly triggered only in the presence of a target protein.

    The molecular chain reaction is driven by a cycle of DNA binding events. The process begins with a DNA key divided into two parts. If the target protein is present, the two parts bind together to form a DNA complex. The formation of the DNA complex generates DNA signaling molecules, which in turn generates the same DNA complex, leading to more signaling molecules, thus propagating repeated cycles.

    “By cutting the DNA ‘key’ into two parts, we found that each part could not catalyze or ‘open’ the reaction separately, but only when a protein acted as glue — essentially bridging the parts together, does the DNA key became functional again,” said Kim, a member of Di Carlo’s laboratory.

    The UCLA team’s findings build on previous work that employed this enzyme-free mechanism of nucleic acid amplification to detect DNA.

    “Unlike previous approaches to achieve an amplified readout of proteins, such as the proximity ligation assay, this approach does not require multiple enzymes, longer polymerization-based enzymatic reactions, or temperature control to amplify signal,” Di Carlo said. “In fact the new assay operates at room temperature and achieves results in about 10 minutes.”

    The team demonstrated the approach with two target proteins — streptavidin, widely used as a test protein for new diagnostic assays, and influenza nucleoprotein, which is a protein associated with the influenza virus.

    In the long term the team aims to combine the technique with portable readers that could be particularly beneficial in clinics in resource-poor areas.

    “Because the technique requires fewer steps than other assays, it can have a significant impact on distributed diagnostics and public health reporting, especially in combination with cost-effective portable and networked reader technology that our lab is developing,” Ozcan said.

    The team demonstrated a synergistic handheld microplate reader suitable for protein diagnostic assays based on a cellphone’s optical and computational systems earlier this year.

    Garner, who is also the associate director of the clinical microbiology lab at UCLA Health, emphasized the broad application of the technique. “Although demonstrated initially in detecting protein associated with flu, we envision the approach can be generalized to a range of protein biomarkers associated with infectious diseases and cancer,” said Garner. He noted it could be configured to detect diseases such as Zika or Ebola.

    The researchers emphasized that additional work is required to adapt the assay to complex clinical samples that may have other interfering compounds, and further optimization of the reagents for the assay can enhance performance.

    This interdisciplinary work was supported through a team science grant from the National Science Foundation Emerging Frontiers in Research and Innovation program.

    See the full article here .

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    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

  • richardmitnick 2:55 pm on August 29, 2016 Permalink | Reply
    Tags: , , Medicine, ,   

    From JHU: “Scientists screen existing drugs in hopes of fast-tracking Zika treatment” 

    Johns Hopkins
    Johns Hopkins University

    Rachel Butch

    A specialized drug screen test using lab-grown human cells has revealed two classes of compounds already in the pharmaceutical arsenal that may work against mosquito-borne Zika virus infections, scientists say.

    Zika virus infection in cell death in human forebrain organoids. Image credit: Xuyu Qian, Johns Hopkins University

    In a summary of their work, published today in Nature Medicine, the investigators say they screened 6,000 existing compounds currently in late-stage clinical trials or already approved for human use for other conditions. The screening process identified several compounds that showed the ability to hinder or halt the progress of the Zika virus in lab-grown human neural cells.

    The research collaboration includes teams from the Johns Hopkins University School of Medicine, the National Institutes of Health, and Florida State University.

    “It takes years, if not decades, to develop a new drug,” says Hongjun Song, director of the Stem Cell Biology Program in the Institute of Cell Engineering at Johns Hopkins. “In this sort of global health emergency, we don’t have that kind of time.”

    Adds Guo-li Ming, professor of neurology at JHU’s School of Medicine: “Instead of using new drugs, we chose to screen existing drugs. In this way, we hope to create a therapy much more quickly.”

    The current outbreak of Zika, which began in South America last year, is known to be responsible for an increase in cases of microcephaly—a severe birth defect in which afflicted infants are born with underdeveloped brains. In the continental United States, there have been a total of 2,260 reported cases of Zika. Though most cases are associated with travel, 43 cases of local transmission have been reported in Florida, in the Miami area. In addition, Puerto Rico has reported 7,855 locally transmitted cases, spurring the Obama administration to declare a public health emergency in the territory on Aug. 12.

    The Zika virus is commonly transmitted from mosquito bites or from an infected person to an uninfected person through sexual contact. Despite the potential effects of infection, only one in four infected people will present symptoms if Zika infection, allowing the virus to spread rapidly in areas with local transmission. Because of this, the CDC recommends all pregnant women with ongoing risk of Zika infection, including residence or frequent travel to areas with active Zika virus transmission, receive screening throughout their pregnancy.

    Many research groups are fast tracking the development of vaccines, treatments, and mosquito-control measures to combat further spread of the virus.

    The new findings are an extension of previous work by the same research team, which found that Zika mainly targets specialized stem cells that give rise to neurons in the brain’s outer layer, the cortex. The researchers observed Zika’s effects in two- and three-dimensional cell cultures called “mini-brains,” which share structures with the human brain and allow researchers to study the effects of Zika in a more accurate model for human infection.

    In the current study, the research team exposed similar cell cultures to the Zika virus and the drugs one at a time, measuring for indicators of cell death, including caspase-3 activity, a chemical marker of cell death, and ATP, a molecule whose presence is indicative of cell vitality.

    Typically, after Zika infection, the damage done to neural cells is “dramatic and irreversible,” says Hengli Tang, professor of biological sciences at Florida State University. However, some of the compounds tested allowed the cells to survive longer and, in some cases, fully recover from infections.

    Further analysis of the surviving cells, Ming says, showed that the promising drugs could be divided into two classes: neuroprotective drugs, which prevent the activation of mechanisms that cause cell death; and antiviral drugs, which slow or stop viral infection or replication.

    Overall, Song says, three drugs showed robust enough results to warrant further study:

    PHA-690509, an investigational compound with antiviral properties
    emricasan, now in clinical trials to reduce liver damage from hepatitis C virus and shown to have neuroprotective effects
    niclosamide, a drug already used in humans and livestock to combat parasitic infections, which worked as an antiviral agent in these experiments

    Song cautioned that the three drugs “are very effective against Zika in the dish, but we don’t know if they can work in humans in the same way.” For example, he says, although niclosamide can safely treat parasites in the human gastrointestinal tract, scientists have not yet determined if the drug can even penetrate the central nervous system of adults or a fetus inside a carrier’s womb to treat the brain cells targeted by Zika.

    Nor, he says, do they know if the drugs would address the wide range of effects of Zika infection, which include microcephaly in fetuses and temporary paralysis from Guillain-Barre syndrome in adults.

    “To address these questions, additional studies need to be done in animal models as well as humans to demonstrate their ability to treat Zika infection,” Ming says. “So we could still be years away from finding a treatment that works.”

    The researchers say their next steps include testing the efficacy of these drugs in animal models to see if they have the ability to combat Zika in vivo.

    See the full article here .


    There is a new project at World Community Grid [WCG] called OpenZika.
    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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    Johns Hopkins Campus

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

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

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

  • richardmitnick 12:13 pm on August 26, 2016 Permalink | Reply
    Tags: , Breast milk sugar may protect babies against deadly infection, Group B streptococcus, , Medicine   

    From ICL: “Breast milk sugar may protect babies against deadly infection” 

    Imperial College London
    Imperial College London

    26 August 2016
    Kate Wighton

    A type of sugar found in some women’s breast milk may protect babies from a potentially life threatening bacterium called Group B streptococcus.

    These bacteria are a common cause of meningitis in newborns and the leading cause of infection in the first three months of life in the UK and globally.

    The new research, on 183 women in The Gambia and published in the journal Clinical and Translational Immunology, suggests a sugar found in some women’s breast milk protect babies against the bacteria.

    The bug is carried naturally in the vagina and bowels by up to one in three women and can be transferred to the baby during childbirth or in breast milk. In the UK pregnant women deemed high risk are offered a test for the bacteria, or women can pay privately. This test consists of a swab a few weeks before a woman’s due date. However there is still a chance of a woman picking up the bacteria in her gut at some point between the test and giving birth (once the bug gets into the gut of the mother or baby it can trigger an infection).

    However, the new research, from the Centre for International Child Health at Imperial, found that naturally-occurring sugars in a woman’s breast milk may have protective effects against Group B streptococcus.

    Each woman’s breast milk contains a mixture of many different types of sugar, called human milk oligosaccharides. These are not digested in the baby’s tummy and act as food for the ‘friendly bacteria’ in a baby’s intestine.

    The type of sugars a woman produces in her breast milk are partly dictated by her genetic make-up. A type of genetic system in particular, called the Lewis antigen system (which is involved in making the ABO blood group), plays an important role in determining breast milk sugars.

    In the study, the team tested all the mothers’ breast milk for the sugars that are known to be controlled by these Lewis genes. They also tested women and their babies for Group B streptococcus at birth, six days later, and then between 60 and 89 days after birth.

    The team found women who produced breast milk sugars linked to the Lewis gene were less likely to have the bacteria in their gut, and their babies were also less likely to get the bacteria from their mothers at birth.

    In addition, among the babies who had the bacteria in their guts at birth, the infants whose mothers produced a specific sugar in their breast milk, called lacto-n-difucohexaose I, were more likely to have cleared the bacteria from their body by 60-89 days after birth. This suggests this breast milk sugar, which is linked to the Lewis gene, may have a protective effect.

    The researchers then went on to show in the laboratory that breast milk containing this particular sugar – lacto-n-difucohexaose I – was better at killing the Group B streptococcus bacteria compared to breast milk without this specific sugar.

    Around half of all women in the world are thought to produce the sugar lacto-N-difucohexaose I.

    Dr Nicholas Andreas, lead author of the research from the Department of Medicine at Imperial said: “Although this is early-stage research it demonstrates the complexity of breast milk, and the benefits it may have for the baby. Increasingly, research is suggesting these breast milk sugars (human milk oligosaccharides) may protect against infections in the newborn, such as rotavirus and Group B streptococcus, as well as boosting a child’s “friendly” gut bacteria.”

    He added the presence of these sugars allows “friendly” bacteria to flourish and out-compete any harmful bacteria that may be in the youngster’s gut, such as Group B streptococcus.

    The sugars are also thought to act as decoys, and fool the bacteria into thinking the sugar is a type of human cell that can be invaded. The bacteria latch onto the sugar and is then excreted by the body. This may help protect the baby from infection until their own immune system is more mature to fight off the “bad bugs” at around six months of age.

    The team hope their findings might lead to new treatments to protect mothers and babies from infections. The researchers raise the possibility of giving specific breast milk sugar supplements to pregnant and breast-feeding women who do not carry the active Lewis gene. This may help prevent harmful bacteria getting into the baby’s gut at birth and in the first weeks of life.

    Some companies are already exploring adding such sugars to formula milk, but Dr Andreas cautioned it would be difficult to replicate the mix of sugars found in breast milk: “These experimental formulas only contain a couple of these compounds, whereas human breast milk contains dozens of different types. Furthermore, the quantity of sugars produced by the mother changes as the baby ages so that a newborn baby will receive a higher amount of sugars in the breast milk compared to a six-month-old.”

    Dr Andreas, who is a post-doctoral fellow at the Centre for International Child Health at Imperial, also suggested that testing new mothers’ blood for the Lewis gene may be beneficial: “If we know whether a mother is colonised with Group B streptococcus and know if she carries an active copy of the Lewis gene, it may give us an indication of how likely she is to pass the bacteria on to her baby, and more personalised preventive measures could be applied.”

    The work was supported by the Medical Research Council at the MRC Unit The Gambia, the Wellcome Trust, and the Thrasher Research Fund.

    See the full article here .

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    Imperial College London

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

  • richardmitnick 10:54 am on August 26, 2016 Permalink | Reply
    Tags: , Medicine, , Sex reshapes the immune system to boost chances of pregnancy   

    From New Scientist: “Sex reshapes the immune system to boost chances of pregnancy” 


    New Scientist

    26 August 2016
    Alice Klein

    Sending messages of acceptance. Sciepro/Science Photo Library

    Semen does more than fertilise eggs. In mice, it seems to prime the female’s immune system for pregnancy, making it more likely that an embryo will successfully implant in the womb. It appears to prompt similar changes in women, a finding that could explain why IVF is more successful in during treatment.

    Sarah Robertson at the University of Adelaide, Australia, and her colleagues found that each time a female mouse copulates, it caused the release of immune cells called regulatory T-cells, which are known to dampen down inflammation in the body.

    This process may be important for allowing embryos to implant in the womb, rather than being rejected as a foreign body. In people, low regulatory T-cell counts are linked to several reproductive problems, including unexplained infertility, miscarriage, pre-eclampsia and pre-term labour.

    Examining the cervix in women, the team found signs that semen does seem to prompt immune system changes in people too. Shortly after sex, they detected the cervix begins to release immune signalling molecules, which may be a sign of increased levels of regulatory T-cells.

    “It’s as if the seminal fluid is a Trojan horse that activates the immune cells to get things ready for conception,” says Robertson.

    As well as making the embryo more likely to successfully implant in the womb lining, it’s possible that such effects also minimise the chances of a woman’s body rejecting the fetus later on in pregnancy, she says. Women who conceive after limited sexual activity are , she adds.

    IVF help

    The findings, presented at the International Congress of Immunology in Australia this week, fit with observations that semen contains several signaling molecules – including cytokines, prostaglandins, and hormones – that can have an effect on female tissue.

    The discovery has implications for IVF. After a woman’s eggs have been fertilised in the lab, an embryo is chosen for implantation and is surgically inserted into the womb. This is one of the points where IVF can fail, if an embryo is unable to implant in a woman’s uterine lining.

    Many fertility clinics advise couples to abstain from sex during IVF treatment to minimise risk of infection from seminal fluid during the implantation surgery. This is a small risk outweighed by the benefits semen can have for the female immune system, Robertson says.

    This is supported by a recent review of studies that concluded that sex during IVF improves embryo implantation rates by 23 per cent. “I think it’s really good for couples to know that there’s something they can do to help their chances – it allows them to take a bit of control back,” says Robertson.

    Peter Illingworth of IVF Australia says the evidence is compelling. “I personally always say to IVF patients: ‘if you want to have sex, just have sex’.” But many couples choose not to during the treatment because IVF causes a lot of discomfort, he says. “If you’ve got ovaries the size of baseballs, sex is a much less appealing prospect.”

    Conception delay

    The effect of semen on a woman’s immune system could also help explain why most couples do not fall pregnant straight away, says Robertson. “In humans, it seems that at least three months of sexual cohabitation is required to give you the priming that you need,” she says.

    If low levels of regulatory T-cells are for a cause of infertility, therapies that increase them may help women who have been trying unsuccessfully to get pregnant for a long time. Treatments like these are currently being developed for immune conditions like graft-versus-host disease, but they haven’t been tested for fertility yet.

    “Our results suggest that the first-line approach to treating infertility should be to tell people to go home and practise,” Robertson says. “But if that doesn’t work, tackling regulatory T cells may be the way to go.”

    See the full article here .

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  • richardmitnick 8:28 am on August 26, 2016 Permalink | Reply
    Tags: ‘Out-of-body’ training boosts heart-surgery residents’ skills, Medicine, Simulation anatomy,   

    From U Washington: “‘Out-of-body’ training boosts heart-surgery residents’ skills” 

    U Washington

    University of Washington

    Brian Donohue

    A cardiothoracic surgeon in training practices on a medical model at UW Medicine’s WWAMI Institute for Simulation in Healthcare. UW Medicine

    Surgical residents learn their craft mostly in the operating room, watching and assisting mentors with patient procedures until their skills and poise suffice to fly solo.

    Such on-the-job training has been standard forever, but a study published today in The Annals of Thoracic Surgery indicates there might be a better way: simulation.

    “Conventional thinking is that the only place you can learn cardiac surgery skills is in the OR. We found that’s not true,” said UW Medicine cardiothoracic surgeon Nahush Mokadam. He and peers at seven U.S. academic medical centers developed a simulation curriculum and evaluated its benefits to surgical residents.

    Over a span of months, with repeated practice and coaching from faculty mentors, 27 novice-level residents became “expertly skilled,” Mokadam said, in routine procedures such as aortic valve replacement. Residents received detailed instruction in how to address catastrophes during surgery, and then practiced in a fully immersive simulated environment.

    “Practicing surgery outside of the high-stakes, real-patient environment better prepares the trainee. When they get to the operating room, it’s not the first time they’ve practiced or conceptually gone through the steps of a procedure,” Mokadam said.

    The study involved a rigorous, 39-session (four hours/week) course with training modules for three common cardiothoracic surgeries and three adverse events. Simulation technologies ranged from low-fidelity plastic models to real tissue and pig hearts that paralleled the experience of surgery on actual patients.

    Cardiothoracic surgery residents improved in all technical skills evaluated, with perfect or near-perfect performance after about 110 hours of simulation training per resident, the authors said. The course also significantly improved trainees’ decisions and communications.

    A surgeon practices coronary artery bypass grafting on a pig heart at the WWAMI Institute for Simulation in Healthcare. UW Medicine

    The study’s lead investigator, Dr. Richard Feins of the University of North Carolina, said the modern operating room is too fast-paced and has too many competing priorities to be the only place to train residents.

    “One would never expect to produce an outstanding basketball team if the players could only develop their skills during a game. But that is essentially what the apprentice model in surgery does. We have shown there is a better way.”

    The value of the course was also evident in participants’ feedback, gathered in a survey: Among respondents, 85 percent of residents and 100 percent of faculty felt more comfortable with the residents’ OR performance.

    Dr. Josh Hermsen, now a UW Medicine attending cardiothoracic surgeon, was among the residents who took the course at the WWAMI Institute for Simulation in Healthcare. He said the course’s biggest advantage was its low-risk, low-intensity environment, which encouraged the exploration of concepts and gave time for lessons to sink in.

    “From the get-go, I felt like I had a framework to think about the cases we were doing,” Hermsen said. “What we were doing in the OR made a lot more sense. One big plus was learning the nuts and bolts of the heart-lung machine, which looks like a bunch of tubes going every which way; it can be confusing and even distracting in surgery.

    “And there’s learning,” he continued, “that comes from things that aren’t spelled out in the curriculum. The instructors can talk about ‘What happens if you do that?’ or ‘What happens if you encounter this?’ You talk about it there, and when it happens in the OR, you know how to deal with it.”

    Such validation supports the efficacy of simulation training, Mokadam said, even though the participant-focused results cannot be scientifically said to improve patient care.

    “We have a pile of data indicating that simulation training makes surgeons highly proficient and more able to address adverse events,” he said. “We think it’s not a stretch to suggest that this curriculum likely would improve patient safety and outcomes.”

    In addition to Drs. Fein and Mokadam, the Cardiac Surgery Simulation Consortium includes Drs. Harold Burkhart of the Mayo Clinic; John Conte of Johns Hopkins University; James Fann of Stanford University; George Hicks of the University of Rochester; Jonathan Nesbitt of Vanderbilt University; and Robert Shen of the Mayo Clinic; and Jennifer Walker of Massachusetts General Hospital.

    Access the full-text research: Study 1 Study 2

    See the full article here .

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

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

  • richardmitnick 8:14 am on August 26, 2016 Permalink | Reply
    Tags: , , Medicine,   

    From UCLA: “UCLA-led study sheds new light on the complex genetics of autism” 

    UCLA bloc


    August 25, 2016
    Jim Schnabel

    The UCLA-led study uncovered more than a dozen potential new autism spectrum disorder risk genes, one of them linked to delays in language ability. Dr. Richard Feldman/National Cancer Institute

    A new study led by UCLA scientists shows that in families with multiple children on the autism spectrum, the pattern of genetic factors is different from that seen in families with just one affected child.

    The study focused on genetic changes known as copy-number variations (CNVs), which are losses or gains of normal DNA. Previous research has linked non-inherited CNVs, which originate as defects in the sperm or egg cell from which the affected child is conceived, to autism spectrum disorder in children whose siblings are not affected.

    The research findings included the discovery of more than a dozen promising new candidates for genes linked to the risk of autism spectrum disorders, highlighting the complexity of genetic factors in the disorders. The findings provide a better picture of how genetic variation contributes to autism disorders, and could perhaps point to a possible new target for future therapies. The study appears in the Aug. 25 issue of the American Journal of Human Genetics.

    The researchers found that, among children with an autism spectrum disorder who have siblings with autism disorders, inherited copy-number variations had a stronger influence than non-inherited CNVs. This was expected, but had previously not been demonstrated.

    Although the researchers expected inherited factors to appear to play a greater role in families in which more than one child has an autism spectrum disorder, they were surprised by another observation in these families: When an affected child has an inherited genetic variation that is known to be an autism spectrum disorder risk factor, it is seldom the case that all his affected siblings have that same variation.

    “It’s actually the exception rather than the rule,” said principal investigator Dr. Daniel Geschwind, the Gordon and Virginia MacDonald Distinguished Professor of Human Genetics at the David Geffen School of Medicine at UCLA. “So for example, there are families in which only two of three kids have the rare CNV inherited from the parent, yet they all have been diagnosed with an autism disorder. One might have expected all three to inherit this major risk factor.”

    The study arose from a long-running project by Geschwind and collaborators to gather DNA and clinical data on families with more than one child with autism spectrum disorder. These are known as “multiplex families.” Most autism genetics studies have focused on families with just one affected child, known as “simplex families,” because researchers predicted that certain types of disease-related DNA changes were in principle easier to detect in such families.

    The relative exclusion of multiplex families, which account for about 11 percent of families with children who have an autism spectrum disorder, may have distorted the picture of how DNA changes contribute to autism disorders. Most obviously, cases of autism spectrum disorder diagnosed in siblings, which appear to run in the family, would be expected to result more from heritable genetic variations than non-inherited CNVs. Heritability is the extent to which genetic differences contribute to observed physical differences.

    One possible explanation for the finding that autistic siblings in a family usually do not all have the same disease-linked genetic variation, Geschwind said, is that lightning has indeed struck twice — in the form of an unlucky non-inherited mutation that accounts for an autism spectrum disorder in a child who lacks inherited risk factors found in siblings.

    Another possibility is that the autism spectrum disorder arises in the siblings mostly from other, harder-to-find factors, for example common or rare inherited variation in many genes, so that the presence or absence of a large, inherited copy-number variation influences only the severity of the disorder.

    The analysis is based on the final collection of data on 1,532 ASD families, which is known as the Autism Genetic Resource Exchange. About 80 percent of the families in the database are multiplex.

    “This is the largest study of its kind in families with multiple autism spectrum disorder children, and it shows that looking at such families can provide significant new insights,” said Geschwind, who is also a professor of neurology and psychiatry.

    Of the potential new autism spectrum disorder risk genes discovered by the researchers, one of them, NR4A2, is linked to some rare cases of autism disorder with delays in language ability. The language connection, Geschwind said, fits with a previous finding from his laboratory that NR4A2 is expressed in the human brain in areas involved in language development, specifically the temporal lobe.

    Geschwind emphasized that the complex genetic underpinnings of autism spectrum disorder in multiplex families need to be better characterized with larger studies of these families. “There are a lot of multiplex families out there waiting to be studied, but unfortunately it seems there is no effort now to study these families on a larger scale,” Geschwind said.

    The lead author of the study, who performed most of the analyses, was Virpi Leppa, a postdoctoral researcher in the Geschwind Laboratory.

    The research was part of a collaborative effort including researchers from Yale University, University of California, San Francisco, Washington University at St. Louis, and other institutions.

    Funding was provided by the National Institute for Mental Health (R01 MH081754, R01 MH100027, R01 MH074090, R01 MH06454701S1). The Autism Genetic Resource Exchange was initially supported by the Cure Autism Now foundation, which later merged with another organization, Autism Speaks.

    See the full article here .

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    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

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