252 research outputs found

    Suppression of Sensorimotor Alpha Power Associated With Pain Expressed by an Avatar: A Preliminary EEG Study

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    Several studies using functional magnetic resonance imaging (fMRI) showed that empathic capabilities are associated with the activation (and deactivation) of relatively specific neural circuits. A growing number of electroencephalography studies also suggest that it might be useful to assess empathy. The main goal of this study was to use quantitative electroencephalography (qEEG) to test whether observation of pain expressed by an avatar (virtual reality) induces a suppression of alpha waves over sensorimotor cortical areas, as it is observed with human stimuli. Not only was it the case, but also the magnitude of alpha suppression was correlated with perspective-taking capacity of participants. Both empathy levels and magnitude of sensorimotor alpha suppression (SAS) were significantly higher in women than men. Interestingly, a significant interaction emerged between levels of individual empathy and specificity of experimental instructions, where SAS in participants with good perspective-taking was higher during passive observation of the distressed avatar, while the opposite was true during an active (trying to understand) condition. These results suggest that: (1) synthetic characters are able to elicit SAS; (2) SAS is indeed associated with perspective-taking capacities; (3) Persons with poorer perspective-taking capacities can show significant SAS when proper instructions are provided. Therefore, qEEG represents a low-cost objective approach to measure perspective-taking abilities

    Predicting enhanced absorption of light gases in polyethylene using simplified PC-SAFT and SAFT-VR

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    International audienceAbsorption of light gases in polyethylene (PE) is studied using two versions of the Statistical Associating Fluid Theory (SAFT): SAFT for chain molecules with attractive potentials of variable range (VR) and simplified perturbed-chain (PC) SAFT. Emphasis is placed on the light gases typically present during ethylene polymerisation in the gas-phase reactor (GPR) process. The two approaches are validated using experimental binary-mixture data for gas absorbed in PE, and predictions are made for mixtures of more components. For most cases studied both SAFT versions perform equally well. For the case of ternary mixtures of two gases with PE, it is predicted that the less-volatile of the two gases acts to enhance the absorption of the more-volatile gas, while the more-volatile gas inhibits the absorption of the less-volatile gas. This general behaviour is also predicted in mixtures containing more gases, such as typical reactor mixtures. The magnitude of the effect may vary considerably, depending on the relative proximity of the gas-mixture saturation pressure to the reactor pressure; for example it is predicted that the absorption of ethylene may be approximately doubled if diluent gases, propane or nitrogen, are partially or completely replaced by less-volatile butane or pentane for a reactor pressure similar to 2 MPa. In the case of a co-polymerisation reaction, it is predicted that increases in absorption of both co-monomers may be obtained in roughly equal proportion. Our findings cast light on the so-called co-monomer effect, in which substantial increases in the rate of ethylene polymerisation are observed in the presence of hexene co-monomer, while suggesting that the effect is more general and not restricted to co-monomer. For example, similar rate increases may be expected in the presence of, e.g., pentane instead of hexene, but without the change in the branch structure of the produced polymer that is inevitable when the amount of co-monomer is increased

    Diverse perspectives on interdisciplinarity from the Members of the College of the Royal Society of Canada

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    Various multiple-disciplinary terms and concepts (although most commonly “interdisciplinarity”, which is used herein) are used to frame education, scholarship, research, and interactions within and outside academia. In principle, the premise of interdisciplinarity may appear to have many strengths; yet, the extent to which interdisciplinarity is embraced by the current generation of academics, the benefits and risks for doing so, and the barriers and facilitators to achieving interdisciplinarity represent inherent challenges. Much has been written on the topic of interdisciplinarity, but to our knowledge there have been few attempts to consider and present diverse perspectives from scholars, artists, and scientists in a cohesive manner. As a team of 57 members from the Canadian College of New Scholars, Artists, and Scientists of the Royal Society of Canada (the College) who self-identify as being engaged or interested in interdisciplinarity, we provide diverse intellectual, cultural, and social perspectives. The goal of this paper is to share our collective wisdom on this topic with the broader community and to stimulate discourse and debate on the merits and challenges associated with interdisciplinarity. Perhaps the clearest message emerging from this exercise is that working across established boundaries of scholarly communities is rewarding, necessary, and is more likely to result in impact. However, there are barriers that limit the ease with which this can occur (e.g., lack of institutional structures and funding to facilitate cross-disciplinary exploration). Occasionally, there can be significant risk associated with doing interdisciplinary work (e.g., lack of adequate measurement or recognition of work by disciplinary peers). Solving many of the world’s complex and pressing problems (e.g., climate change, sustainable agriculture, the burden of chronic disease, and aging populations) demand thinking and working across long-standing, but in some ways restrictive, academic boundaries. Academic institutions and key support structures, especially funding bodies, will play an important role in helping to realize what is readily apparent to all who contributed to this paper—that interdisciplinarity is essential for solving complex problems; it is the new norm. Failure to empower and encourage those doing this research will serve as a great impediment to training, knowledge, and addressing societal issues

    Understanding Human-Plasmodium falciparum Immune Interactions Uncovers the Immunological Role of Worms

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    BACKGROUND: Former studies have pointed to a monocyte-dependent effect of antibodies in protection against malaria and thereby to cytophilic antibodies IgG1 and IgG3, which trigger monocyte receptors. Field investigations have further documented that a switch from non-cytophilic to cytophilic classes of antimalarial antibodies was associated with protection. The hypothesis that the non-cytophilic isotype imbalance could be related to concomittant helminthic infections was supported by several interventions and case-control studies. METHODS AND FINDINGS: We investigated here the hypothesis that the delayed acquisition of immunity to malaria could be related to a worm-induced Th2 drive on antimalarial immune responses. IgG1 to IgG4 responses against 6 different parasite-derived antigens were analyzed in sera from 203 Senegalese children, half carrying intestinal worms, presenting 421 clinical malaria attacks over 51 months. Results show a significant correlation between the occurrence of malaria attacks, worm carriage (particularly that of hookworms) and a decrease in cytophilic IgG1 and IgG3 responses and an increase in non-cytophilic IgG4 response to the merozoite stage protein 3 (MSP3) vaccine candidate. CONCLUSION: The results confirm the association with protection of anti-MSP3 cytophilic responses, confirm in one additional setting that worms increase malaria morbidity and show a Th2 worm-driven pattern of anti-malarial immune responses. They document why large anthelminthic mass treatments may be worth being assessed as malaria control policies

    IRGM Is a Common Target of RNA Viruses that Subvert the Autophagy Network

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    Autophagy is a conserved degradative pathway used as a host defense mechanism against intracellular pathogens. However, several viruses can evade or subvert autophagy to insure their own replication. Nevertheless, the molecular details of viral interaction with autophagy remain largely unknown. We have determined the ability of 83 proteins of several families of RNA viruses (Paramyxoviridae, Flaviviridae, Orthomyxoviridae, Retroviridae and Togaviridae), to interact with 44 human autophagy-associated proteins using yeast two-hybrid and bioinformatic analysis. We found that the autophagy network is highly targeted by RNA viruses. Although central to autophagy, targeted proteins have also a high number of connections with proteins of other cellular functions. Interestingly, immunity-associated GTPase family M (IRGM), the most targeted protein, was found to interact with the autophagy-associated proteins ATG5, ATG10, MAP1CL3C and SH3GLB1. Strikingly, reduction of IRGM expression using small interfering RNA impairs both Measles virus (MeV), Hepatitis C virus (HCV) and human immunodeficiency virus-1 (HIV-1)-induced autophagy and viral particle production. Moreover we found that the expression of IRGM-interacting MeV-C, HCV-NS3 or HIV-NEF proteins per se is sufficient to induce autophagy, through an IRGM dependent pathway. Our work reveals an unexpected role of IRGM in virus-induced autophagy and suggests that several different families of RNA viruses may use common strategies to manipulate autophagy to improve viral infectivity

    Beth Levine in memoriam

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    Beth Levine was born on 7 April 1960 in Newark, New Jersey. She went to college at Brown University where she received an A.B. Magna Cum Laude, and she attended medical school at Cornell University Medical College, receiving her MD in 1986. She completed her internship and residency in Internal Medicine at Mount Sinai Hospital in New York, and her fellowship in Infectious Diseases at The Johns Hopkins Hospital. Most recently, Beth was a Professor of Internal Medicine and Microbiology, Director of the Center for Autophagy Research, and holder of the Charles Sprague Distinguished Chair in Biomedical Science at the University of Texas Southwestern Medical Center in Dallas. Beth died on 15 June 2020 from cancer. Beth is survived by her husband, Milton Packer, and their two children, Rachel (26 years old) and Ben (25 years old). Dr. Levine was as an international leader in the field of autophagy research. Her laboratory identified the mammalian autophagy gene BECN1/beclin 1; identified conserved mechanisms underlying the regulation of autophagy (e.g. BCL2-BECN1 complex formation, insulin-like signaling, EGFR, ERBB2/HER2 and AKT1-mediated BECN1 phosphosphorylation); and provided the first evidence that autophagy genes are important in antiviral host defense, tumor suppression, lifespan extension, apoptotic corpse clearance, metazoan development, Na,K-ATPase-regulated cell death, and the beneficial metabolic effects of exercise. She developed a potent autophagy-inducing cell permeable peptide, Tat-beclin 1, which has potential therapeutic applications in a range of diseases. She was a founding Associate Editor of the journal Autophagy and an editorial board member of Cell and Cell Host & Microbe. She has received numerous awards/honors in recognition of her scientific achievement, including: The American Cancer Society Junior Faculty Research Award (1994); election into the American Society of Clinical Investigation (2000); the Ellison Medical Foundation Senior Scholars Award in Global Infectious Diseases (2004); elected member, American Association of Physicians (2005); appointment as a Howard Hughes Medical Institute Investigator (2008); Edith and Peter O’Donnell Award in Medicine (2008); elected fellow, American Association for the Advancement of Science (2012); election into the National Academy of Sciences (2013); election into the Academy of Medicine, Engineering and Science of Texas (2013); the ASCI Stanley J. Korsmeyer Award (2014); Phyllis T. Bodel Women in Medicine Award, Yale University School of Medicine (2018); recipient, Barcroft Medal, Queen’s University Belfast (2018).Fil: An, Zhenyi. No especifĂ­ca;Fil: Ballabi, Andrea. No especifĂ­ca;Fil: Bennett, Lynda. No especifĂ­ca;Fil: Boya, Patricia. No especifĂ­ca;Fil: Cecconi, Francesco. No especifĂ­ca;Fil: Chiang, Wei Chung. No especifĂ­ca;Fil: Codogno, Patrice. No especifĂ­ca;Fil: Colombo, Maria Isabel. No especifĂ­ca;Fil: Cuervo, Ana Maria. No especifĂ­ca;Fil: Debnath, Jayanta. No especifĂ­ca;Fil: Deretic, Vojo. No especifĂ­ca;Fil: Dikic, Ivan. No especifĂ­ca;Fil: Dionne, Keith. No especifĂ­ca;Fil: Dong, Xiaonan. No especifĂ­ca;Fil: Elazar, Zvulun. No especifĂ­ca;Fil: Galluzzi, Lorenzo. No especifĂ­ca;Fil: Gentile, Frank. No especifĂ­ca;Fil: Griffin, Diane E.. No especifĂ­ca;Fil: Hansen, Malene. No especifĂ­ca;Fil: Hardwick, J. Marie. No especifĂ­ca;Fil: He, Congcong. No especifĂ­ca;Fil: Huang, Shu Yi. No especifĂ­ca;Fil: Hurley, James. No especifĂ­ca;Fil: Jackson, William T.. No especifĂ­ca;Fil: Jozefiak, Cindy. No especifĂ­ca;Fil: Kitsis, Richard N.. No especifĂ­ca;Fil: Klionsky, Daniel J.. No especifĂ­ca;Fil: Kroemer, Guido. No especifĂ­ca;Fil: Meijer, Alfred J.. No especifĂ­ca;Fil: MelĂ©ndez, Alicia. No especifĂ­ca;Fil: Melino, Gerry. No especifĂ­ca;Fil: Mizushima, Noboru. No especifĂ­ca;Fil: Murphy, Leon O.. No especifĂ­ca;Fil: Nixon, Ralph. No especifĂ­ca;Fil: Orvedahl, Anthony. No especifĂ­ca;Fil: Pattingre, Sophie. No especifĂ­ca;Fil: Piacentini, Mauro. No especifĂ­ca;Fil: Reggiori, Fulvio. No especifĂ­ca;Fil: Ross, Theodora. No especifĂ­ca;Fil: Rubinsztein, David C.. No especifĂ­ca;Fil: Ryan, Kevin. No especifĂ­ca;Fil: Sadoshima, Junichi. No especifĂ­ca;Fil: Schreiber, Stuart L.. No especifĂ­ca;Fil: Scott, Frederick. No especifĂ­ca;Fil: Sebti, Salwa. No especifĂ­ca;Fil: Shiloh, Michael. No especifĂ­ca;Fil: Shoji, Sanae. No especifĂ­ca;Fil: Simonsen, Anne. No especifĂ­ca;Fil: Smith, Haley. No especifĂ­ca;Fil: Sumpter, Kathryn M.. No especifĂ­ca;Fil: Thompson, Craig B.. No especifĂ­ca;Fil: Thorburn, Andrew. No especifĂ­ca;Fil: Thumm, Michael. No especifĂ­ca;Fil: Tooze, Sharon. No especifĂ­ca;Fil: Vaccaro, Maria Ines. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de BioquĂ­mica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de BioquĂ­mica y Medicina Molecular; ArgentinaFil: Virgin, Herbert W.. No especifĂ­ca;Fil: Wang, Fei. No especifĂ­ca;Fil: White, Eileen. No especifĂ­ca;Fil: Xavier, Ramnik J.. No especifĂ­ca;Fil: Yoshimori, Tamotsu. No especifĂ­ca;Fil: Yuan, Junying. No especifĂ­ca;Fil: Yue, Zhenyu. No especifĂ­ca;Fil: Zhong, Qing. No especifĂ­ca

    Measurement of the Tau Lepton Polarisation at LEP2

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    A first measurement of the average polarisation P_tau of tau leptons produced in e+e- annihilation at energies significantly above the Z resonance is presented. The polarisation is determined from the kinematic spectra of tau hadronic decays. The measured value P_tau = -0.164 +/- 0.125 is consistent with the Standard Model prediction for the mean LEP energy of 197 GeV.A first measurement of the average polarisation Pτ of tau leptons produced in e + e − annihilation at energies significantly above the Z resonance is presented. The polarisation is determined from the kinematic spectra of tau hadronic decays. The measured value Pτ=−0.164±0.125 is consistent with the Standard Model prediction for the mean LEP energy of 197 GeV.A first measurement of the average polarisation P_tau of tau leptons produced in e+e- annihilation at energies significantly above the Z resonance is presented. The polarisation is determined from the kinematic spectra of tau hadronic decays. The measured value P_tau = -0.164 +/- 0.125 is consistent with the Standard Model prediction for the mean LEP energy of 197 GeV

    Taxonomy based on science is necessary for global conservation

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    Peer reviewe

    American Gut: an Open Platform for Citizen Science Microbiome Research

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    McDonald D, Hyde E, Debelius JW, et al. American Gut: an Open Platform for Citizen Science Microbiome Research. mSystems. 2018;3(3):e00031-18
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