Roizman B.,The University of Chicago |
Zhou G.,Guangzhou University
Virology | Year: 2015
On entry into the body herpes simplex viruses (HSV) replicate in a series of steps that involves derepression of viral DNA activated by VP16, a virion protein, and sequential transcription of viral genes in a cascade fashion. HSV also enters into neurons in which viral DNA maintained as heterochromatin and with few exceptions viral gene expression is silenced. A third face of the interaction of HSV with its host cells takes place at the moment when the silenced viral genome in neurons is abruptly derepressed. The available data do no reveal evidence that HSV encodes different regulatory programs for each facet of its interaction with its host cells. Rather the data point to significant gaps in our knowledge of the mechanisms by which each facet is initiated and the roles of the infected cells at each facet of the interaction of viral gene products with the host cell. © 2015 Elsevier Inc. Source
News Article | August 30, 2016
This week in Chicago, the Array of Things team begins the first phase of the groundbreaking urban sensing project, installing the first of an eventual 500 nodes on city streets. By measuring data on air quality, climate, traffic and other urban features, these pilot nodes kick off an innovative partnership between the University of Chicago, Argonne National Laboratory and the City of Chicago to better understand, serve and improve cities. Array of Things is designed as a "fitness tracker" for the city, collecting new streams of data on Chicago's environment, infrastructure and activity. This hyper-local open data can help researchers, city officials and software developers study and address critical city challenges, such as preventing urban flooding, improving traffic safety and air quality and assessing the nature and impact of climate change. In the first phase of the project, 50 nodes will be installed in August and September on traffic light poles in The Loop, Pilsen, Logan Square and along Lake Michigan. These nodes will contain sensors for measuring air and surface temperature, barometric pressure, light, vibration, carbon monoxide, nitrogen dioxide, sulfur dioxide, ozone and ambient sound intensity. Two cameras will collect data on vehicle and foot traffic, standing water, sky color and cloud cover. The first two nodes were installed last week at the intersections of Damen and Archer Avenues and Damen Avenue and Cermak Road, where they will collect information on weather, traffic and air quality. A total of 500 nodes will be installed across Chicago by the end of 2018, and additional nodes will be shared with cities across the United States and in countries such as England, Mexico, and Taiwan. "The University of Chicago has a long and flourishing tradition of scholarship that engages with urban life and makes a positive impact," said Robert J. Zimmer, president of the University. "The Array of Things project advances these ideals by gathering a broad scope of data about the urban environment, in a form that researchers, policymakers and residents can use to develop innovative ways of improving our city and urban areas around the world." "The Array of Things project is just one example of the advancements that are possible when the city, university and Argonne combine their diverse and complementary perspectives, experience and expertise," said Argonne Director Peter B. Littlewood. "I'm excited to see the Array of Things fulfill its potential to help make Chicago cleaner, healthier and more livable, and I also look forward to future game-changing collaborations with our local partners." Initial node locations and data applications were determined based on interactions with community organizations and research groups. Eight nodes in Pilsen will contain sensors for tracking air quality and its relationship with asthma and other diseases. Partnerships with the Chicago Loop Alliance and Vision Zero motivated studies of pedestrian and vehicle flow and traffic safety in The Loop neighborhood. And scientists at UChicago and Argonne chose locations along the lake and across the middle of Chicago that will allow for optimal measurements of features related to urban weather and climate change. "The Array of Things is a community technology," said Charlie Catlett, director of the Urban Center and Computation and Data at the University of Chicago and Argonne and the lead investigator of Array of Things. "It's about creating new streams of data that help us understand and address the most critical urban challenges. Where we see an intersection of resident concerns, science interests and policymaker interest, that's where we see opportunity for Array of Things deployment in Chicago." Array of Things will also support City of Chicago efforts to provide smarter and proactive services using predictive analytics and data-driven policy. For example, by tracking the weather conditions leading up to flooding at intersections, city crews can respond more quickly to floods or make infrastructural changes that prevent standing water from accumulating. City departments could also use data on heavy truck traffic and air quality to make decisions about commercial routing that preserves clean air and safe roads in residential neighborhoods. "It's truly doing science in the city and out in the communities. We'll be able to engage with community groups to help them make the data their own and figure out to use it to address the questions they have," said Brenna Berman, Chief Information Officer of the City of Chicago. "You're going to see community groups use this data to understand their communities and neighborhoods better as we all try to build a better life here in Chicago." Data collected by Array of Things nodes will be open, free and available to the public, researchers and developers. After a brief period of testing and calibration, the project will publish data through the City of Chicago Data Portal, open data platform Plenar.io, and via application programming interfaces. As specified by the Array of Things privacy and governance policies, no personally identifiable information will be stored or released by sensor nodes. Array of Things is funded by a $3.1 million grant from the National Science Foundation, with additional investments from Argonne and the Chicago Innovation Exchange. "We at the National Science Foundation are proud to support the Array of Things," said Jim Kurose, head of Computer and Information Science and Engineering at NSF. "The launch of the first nodes will provide important information and data-driven insights about the health of cities and residents, and illustrate how fundamental research is vital to the transformation of our local communities envisioned by the National Smart Cities Initiative." The underlying software and hardware uses the Waggle sensor platforming, designed by Pete Beckman, Rajesh Sankaran and Catlett at Argonne. The node enclosures were designed and manufactured by Product Development Technologies in Lake Zurich, Ill., from original designs by Douglas Pancoast and Satya Mark Basu of the School of the Art Institute of Chicago. AT&T is the project's communications partner, providing all AoT connectivity for Chicago. Array of Things technology was developed with help from industry partners who provided in-kind engineering expertise, including Cisco, Intel, Microsoft, Motorola Solutions, Schneider Electric and Zebra Technologies.
Multiple sclerosis (MS) may be triggered by the death of brain cells that make the insulation around nerve fibers, a surprising new view of the disease reported in a study from Northwestern Medicine and The University of Chicago. And a specially developed nanoparticle prevented MS even after the death of those brain cells, an experiment in the study showed. The nanoparticles are being developed for clinical trials that could lead to new treatments -- without the side effects of current therapies -- in adults. MS can be initiated when damage to the brain destroys the cells that make myelin, the scientists showed. Myelin is the insulating sheath around nerve fibers that enables nerve impulses to be transmitted. The death of these cells, oligodendrocytes, can activate the autoimmune response against myelin, which is the main feature of MS. Oligodendrocytes can possibly be destroyed by developmental abnormalities, viruses, bacterial toxins or environmental pollutants. The scientists also developed the first mouse model of the progressive form of the autoimmune disease, which will enable the testing of new drugs against progressive MS. In the study, nanoparticles creating tolerance to the myelin antigen were administered and prevented progressive MS from developing. The study was published in Nature Neuroscience December 14. The lead investigators are Stephen Miller, Judy Gugenheim Research Professor of Microbiology-Immunology at Northwestern University Feinberg School of Medicine, and Brian Popko, the Jack Miller Professor of Neurological Disorders at the University of Chicago. The nanoparticle technology was developed in Miller’s lab and has been licensed to Cour Pharmaceutical Development Company, which is developing the technology for human trials in autoimmune disease. “We’re encouraged that immune tolerance induced with nanoparticles could stop disease progression in a model of chronic MS as efficiently as it can in progressive-remitting models of MS,” Miller said. The timing of therapy is important, Popko pointed out. “Protecting oligodendrocytes in susceptible individuals might help delay or prevent MS from initiating,” Popko said. “It’s likely that therapeutic strategies that intervene early in the disease process will have greater impact.” In the experiment, scientists developed a genetically engineered mouse model in which the oligodendrocytes died, affecting the animals’ ability to walk. The central nervous system regenerated the myelin-producing cells, enabling the mice to walk again. But about six months later, the MS-like disease came barreling back. This demonstrated the scientists’ theory that the death of oligodendrocytes can initiate MS. In humans, the scientists posit, the disease develops years after the initial injury to the brain. The current prevailing theory is that an event outside of the nervous system triggers MS in susceptible individuals who may have a genetic predisposition to the disease. In these individuals, the immune cells that normally fight infections confuse a component of the myelin sheath as foreign. These confused immune cells enter the brain and begin their mistaken attack on myelin, thus initiating MS. But the new study demonstrates the possibility that MS can begin from the inside out, in which damage to oligodendrocytes in the central nervous system can trigger an immune response directly. Oligodendrocytes are responsible for the maintenance of myelin. If they die, the myelin sheath falls apart. The inside-out hypothesis suggests that when myelin falls apart, the products of its degradation are presented to the immune system as foreign bodies or antigens. The immune system then erroneously views them as invaders and begins a full-scale attack on myelin, initiating MS. An estimated 400,000 people in the U.S. and 2.5 million worldwide have MS. Of those with long-standing disease, 50 to 60 percent have progressive MS. The other authors on the paper are Maria Traka of U of C, and Joseph Podojil and Derrick McCarthy of Northwestern. Miller, a founder and chief of the scientific advisory board of Cour Pharmaceutical, does not receive financial compensation from the company. The research was supported by grants from the Myelin Repair Foundation and the National Multiple Sclerosis Society.
Brain cell death is a possible trigger of multiple sclerosis New study in mice finds the death of a specific class of brain cells triggers an MS like immune response, which can be prevented by nanoparticle therapy
Home > Press > Brain cell death is a possible trigger of multiple sclerosis: New study in mice finds the death of a specific class of brain cells triggers an MS-like immune response, which can be prevented by nanoparticle therapy Abstract: Multiple sclerosis (MS) may be triggered by the death of brain cells that make myelin, the insulation around nerve fibers, according to research on a novel mouse model developed by scientists from the University of Chicago and Northwestern Medicine. The death of these cells initiates an autoimmune response against myelin, the main characteristic of the disease, which leads to MS-like symptoms in mice. This reaction can be prevented, however, through the application of specially developed nanoparticles, even after the loss of those brain cells. The nanoparticles are being developed for clinical trials that could lead to new treatments in humans. The study was published in Nature Neuroscience on Dec. 14, 2015. "Although this was a study in mice, we've shown for the first time one possible mechanism that can trigger MS -- the death of the cells responsible for generating myelin can lead to the activation of an autoimmune response against myelin," said study co-senior author Brian Popko, PhD, Jack Miller Professor of Neurological Disorders at the University of Chicago. "Protecting these cells in susceptible individuals might help delay or prevent MS." Multiple sclerosis is a neurological disease involving an abnormal immune response against myelin, which leads to the progressive deterioration of a wide range of body functions. MS is thought to affect 2.5 million people worldwide, and has unclear causes and no known cure. To study how MS is triggered, Popko, with collaborator Stephen Miller, PhD, Judy Gugenheim Research Professor of Microbiology-Immunology at Northwestern University Feinberg School of Medicine, and their teams developed a genetically engineered mouse model that allowed them to target oligodendrocytes, the brain cells that produce myelin. By specifically killing oligodendrocytes, the team observed MS-like symptoms that affected the ability of the mice to walk. After this initial event, the central nervous systems of the mice regenerated their myelin-producing cells, enabling them to walk again. But about six months later, the MS-like symptoms came barreling back. "To our knowledge, this is the first evidence that oligodendrocyte death can trigger myelin autoimmunity, initiating inflammation and tissue damage in the central nervous system during MS," said study co-author Maria Traka, PhD, research associate professor in neurology at the University of Chicago. Possible causes of oligodendrocyte death are developmental abnormalities, viruses, bacterial toxins or environmental pollutants. In humans, the researchers hypothesize MS could develop years after an initial injury to the brain triggers oligodendrocyte death. The mouse model also enabled the testing of new drugs against progressive MS. In the study, nanoparticles creating tolerance to the myelin antigen were administered and prevented progressive MS from developing. The nanoparticle technology was developed in Miller's lab and has been licensed to Cour Pharmaceutical Development Company, which is developing the technology for human trials in autoimmune disease. "We're encouraged that the nanoparticles could stop disease progression in a model of chronic MS as efficiently as it can in progressive-remitting models of MS," Miller said. The timing of therapy is important, Popko pointed out. "It's likely that therapeutic strategies that intervene early in the disease process will have greater impact," he said. Inside-out The current prevailing theory is that an event outside of the nervous system triggers MS in susceptible individuals who may have a genetic predisposition to the disease. In these individuals, the immune cells that normally fight infections confuse a component of the myelin sheath as foreign. These confused immune cells enter the brain and begin their mistaken attack on myelin. But the new study demonstrates the possibility that MS can begin from the inside out, in which damage to oligodendrocytes in the central nervous system can trigger an immune response directly. Oligodendrocytes are responsible for the maintenance of myelin. If they die, the myelin sheath falls apart. The inside-out hypothesis suggests that when myelin falls apart, its components are presented to the immune system as foreign bodies or antigens. The immune system then erroneously views them as invaders and begins a full scale attack on myelin, initiating MS. "It will be exciting to determine the nature of this process in humans--its precise role in MS and whether therapies to prevent it are effective," Popko said. ### The study, 'Oligodendrocyte death results in immune-mediated CNS demyelination,' was supported by the Myelin Repair Foundation and the National Multiple Sclerosis Society. Additional authors include Joseph Podojil and Derrick McCarthy of Northwestern University. Miller, a founder and chief of the Scientific Advisory Board of Cour Pharmaceutical, does not receive financial compensation from the company. Northwestern Medicine is the shared strategic vision of Northwestern Memorial HealthCare and Northwestern University Feinberg School of Medicine to transform the future of healthcare and become one of the nation's premier destinations for patient care. Each day, 26,500 clinical and administrative staff, medical and science faculty and medical students come together with a shared commitment to superior quality, academic excellence, scientific discovery and patient safety. About University of Chicago Medical Center The University of Chicago Medicine & Biological Sciences is one of the nation's leading academic medical institutions. It comprises the Pritzker School of Medicine, a top 10 medical school in the nation; the University of Chicago Biological Sciences Division; and the University of Chicago Medical Center, which recently opened the Center for Care and Discovery, a $700 million specialty medical facility. Twelve Nobel Prize winners in physiology or medicine have been affiliated with the University of Chicago Medicine. For more information, please click If you have a comment, please us. Issuers of news releases, not 7th Wave, Inc. or Nanotechnology Now, are solely responsible for the accuracy of the content.
News Article | September 6, 2016
When companies screen job applicants, they aren't just looking for someone with the skills for the role. They're also looking for an upstanding person—someone who can be trusted and relied upon. But businesses aren't much better than ordinary people at judging character, something most people tend to think they excel at, even when they don't. In other words, that human challenge is also an organizational one, and the standard hiring process isn't always up to the task of meeting it. The unstructured interview is one of the most common tools for hiring supposedly ethical employees. It's an informal meeting with free-flowing questions that tends to differ from candidate to candidate. The conversation usually takes a behavioral turn—questions are rarely job-related. Most interviewers, especially trained human resources professionals, consider themselves well-qualified to give unstructured interviews. And in one sense, they are; evolutionary psychologists believe humans have evolved in order to detect deception—an important survival tool among social creatures like us. But we may overestimate our abilities. One comprehensive review of the data found that, on average, we're barely better lie detectors than sheer chance. The University of Chicago's Nick Epley (in full disclosure, a colleague of mine at Ethical Systems) writes in his book Mindwise that we're much worse at knowing who we can trust than we think (and this even includes people like presidential candidates, whose trustworthiness we scrutinize just about every day for years before casting a vote). A second common hiring tactic are integrity tests—tools used to assess someone's personality, their beliefs about various unethical behaviors, and their self-reports of wrongdoing. But one recent review of the research found that the correlation between integrity tests and counterproductive work behavior was 0.3. That means if we're trying to predict misconduct, these tests reveal less than a tenth of the information they should. Integrity assessments have also been shown to be pretty easy to cheat on. Ironically enough, participants who tried to score higher to get chosen for a job did in fact earn higher scores. And then there are character references. Intuition tells us this type of confirmation is useful. But they're flawed, too—as hiring managers are well aware, a candidate's references are motivated to be positive; you only approach someone as a reference if you know they'll endorse you. What's more, they may unintentionally enable gender bias. Research shows that women are more often described (including by their references) as more communal and less assertive, which can hurt their chances of being hired. So what can you do instead? Applicants are drawn to organizations when there's a match on values. So companies need to develop a strong ethical reputation in order to attract the right types of employees. That means laying the groundwork for recruiting ethical employees well before the hiring process begins. Adam Grant, author of Give and Take and Originals, suggests making it clear to applicants that they'll be evaluated in part on whether they positively influence others in the organization. Usually when people think of hiring for character, they focus on eliminating unethical applicants. But it's just as important to pursue the good that new employees bring. For example, recent research shows that positive energizers—those who lift others up and invigorate them through social interaction—help the workforce become more engaged and higher performing. If new hires can influence existing staff negatively, they can also have the reverse effect. Additionally, research shows that humility can contribute to both individual and organizational performance. That's why it's one of the key characteristics Google actively looks for in candidates. Carnegie Mellon professor Taya Cohen is an expert on hiring ethical employees. One of her most consistent and compelling research findings is that people who are prone to feeling guilty tend to be more ethical and prove to be better team players. As Cohen has written, "The guilt-prone employee doesn’t need to be policed. She will act ethically because of her character." Other studies likewise show this type of employee is more likely to stay committed to the organization. Unstructured interviews may not be particularly useful, but structured interviews—which are job-related and have a scoring key that's based on subject-matter expertise—can be helpful. Interview questions should reflect the specific, desirable characteristics that make somebody thrive in a given role, organization, or industry. In other words, look for the behavioral and temperamental stuff that matters—just know why it matters. We know that ethical people have developed habits, rituals, routines, practices, and mantras to enhance their moral awareness—just as they do with any other of their abilities. So it's important to ask questions that can help you find out whether ethics is a skill they've habituated. As organizational guru Ben Schneider has noted, "The people make the place." Creating an ethical culture is all about bringing in high-character employees. And you can do that just as systematically and rigorously as you test somebody's coding or accounting chops.