59 research outputs found

    Making financial markets safer for consumers: lessons from consumer goods markets and beyond

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    In the wake of the mortgage meltdown, policymakers are discussing how best to protect consumers in financial product markets.Consumer protection ; Financial markets

    Atomic Resonance and Scattering

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    Contains research objectives, summary of research and reports on four research projects.Joint Services Electronics Programs (U. S. Army, U. S. Navy, and U. S. Air Force) under Contract DAAB07-71-C-0300National Science Foundation (Grant GP-28679)National Bureau of Standards (Grant NBS2-9011)U. S. Air Force - Office of Scientific Research (Contract F44620-72-C-0057

    Atomic Resonance and Scattering

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    Contains research objectives and summary of research on eight research projects.National Science Foundation (Grant PHY75-15421-A01)U. S. Air Force - Office of Scientific Research (Grant AFOSR 76-2972)Joint Services Electronics Program (Contract DAAB07-76-C-1400)U. S. Air Force - Office of Scientific Research (Contract F44620-72-C-0057

    Atomic Resonance and Scattering

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    Contains reports on nine research projects.U.S. Energy Research and Development Administration (Contract EG-77-S-02-4370)U. S. Air Force - Office of Scientific Research (Contract F44620-72-C-0057)Joint Services Electronics Program (Contract DAAB07-76-C-1400)National Science Foundation (Grant PHY75-15421-AO1)National Science Foundation (Grant PHY77-09155)National Science Foundation (Grant CHE76-81750)U. S. Air Force - Office of Scientific Research (Grant AFOSR-76-2972A

    Atomic Resonance and Scattering

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    Contains reports on eight research projects.National Science Foundation (Grant PHY77-09155)Joint Services Electronics Program (Contract DAAG29-78-C-0020)U. S. Department of Energy (Grant EG-77-S-02-4370)National Science Foundation (Grant DMR 77-10084)National Aeronautics and Space Administration (Grant NSG-1551)U. S. Air Force - Office of Scientific Research (Grant AFOSR-76-2972)National Science Foundation (Grant CHE76-81750

    Nash Equilibria in Multi-Agent Motor Interactions

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    Social interactions in classic cognitive games like the ultimatum game or the prisoner's dilemma typically lead to Nash equilibria when multiple competitive decision makers with perfect knowledge select optimal strategies. However, in evolutionary game theory it has been shown that Nash equilibria can also arise as attractors in dynamical systems that can describe, for example, the population dynamics of microorganisms. Similar to such evolutionary dynamics, we find that Nash equilibria arise naturally in motor interactions in which players vie for control and try to minimize effort. When confronted with sensorimotor interaction tasks that correspond to the classical prisoner's dilemma and the rope-pulling game, two-player motor interactions led predominantly to Nash solutions. In contrast, when a single player took both roles, playing the sensorimotor game bimanually, cooperative solutions were found. Our methodology opens up a new avenue for the study of human motor interactions within a game theoretic framework, suggesting that the coupling of motor systems can lead to game theoretic solutions

    Phase I Evaluation of Intravenous Ascorbic Acid in Combination with Gemcitabine and Erlotinib in Patients with Metastatic Pancreatic Cancer

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    Preclinical data support further investigation of ascorbic acid in pancreatic cancer. There are currently insufficient safety data in human subjects, particularly when ascorbic acid is combined with chemotherapy.14 subjects with metastatic stage IV pancreatic cancer were recruited to receive an eight week cycle of intravenous ascorbic acid (three infusions per week), using a dose escalation design, along with standard treatment of gemcitabine and erlotinib. Of 14 recruited subjects enrolled, nine completed the study (three in each dosage tier). There were fifteen non-serious adverse events and eight serious adverse events, all likely related to progression of disease or treatment with gemcitabine or erlotinib. Applying RECIST 1.0 criteria, seven of the nine subjects had stable disease while the other two had progressive disease.These initial safety data do not reveal increased toxicity with the addition of ascorbic acid to gemcitabine and erlotinib in pancreatic cancer patients. This, combined with the observed response to treatment, suggests the need for a phase II study of longer duration.Clinicaltrials.gov NCT00954525

    Relief of Preintegration Inhibition and Characterization of Additional Blocks for HIV Replication in Primary Mouse T Cells

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    Development of a small animal model to study HIV replication and pathogenesis has been hampered by the failure of the virus to replicate in non-primate cells. Most studies aimed at achieving replication in murine cells have been limited to fibroblast cell lines, but generating an appropriate model requires overcoming blocks to viral replication in primary T cells. We have studied HIV-1 replication in CD4+ T cells from human CD4/ CCR5/Cyclin T1 transgenic mice. Expression of hCD4 and hCCR5 in mouse CD4+ T cells enabled efficient entry of R5 strain HIV-1. In mouse T cells, HIV-1 underwent reverse transcription and nuclear import as efficiently as in human T cells. In contrast, chromosomal integration of HIV-1 proviral DNA was inefficient in activated mouse T cells. This process was greatly enhanced by providing a secondary T cell receptor (TCR) signal after HIV-1 infection, especially between 12 to 24 h post infection. This effect was specific for primary mouse T cells. The pathways involved in HIV replication appear to be PKCθ−, CARMA1-, and WASp-independent. Treatment with Cyclosporin A (CsA) further relieved the pre-integration block. However, transcription of HIV-1 RNA was still reduced in mouse CD4+ T cells despite expression of the hCyclin T1 transgene. Additional post-transcriptional defects were observed at the levels of Gag expression, Gag processing, Gag release and virus infectivity. Together, these post-integration defects resulted in a dramatically reduced yield of infectious virus (300–500 fold) after a single cycle of HIV-1 replication. This study implies the existence of host factors, in addition to those already identified, that are critical for HIV-1 replication in mouse cells. This study also highlights the differences between primary T cells and cell lines regarding pre-integration steps in the HIV-1 replication cycle

    Gut Microbiome Dysbiosis in Antibiotic-Treated COVID-19 Patients is Associated with Microbial Translocation and Bacteremia

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    Although microbial populations in the gut microbiome are associated with COVID-19 severity, a causal impact on patient health has not been established. Here we provide evidence that gut microbiome dysbiosis is associated with translocation of bacteria into the blood during COVID-19, causing life-threatening secondary infections. We first demonstrate SARS-CoV-2 infection induces gut microbiome dysbiosis in mice, which correlated with alterations to Paneth cells and goblet cells, and markers of barrier permeability. Samples collected from 96 COVID-19 patients at two different clinical sites also revealed substantial gut microbiome dysbiosis, including blooms of opportunistic pathogenic bacterial genera known to include antimicrobial-resistant species. Analysis of blood culture results testing for secondary microbial bloodstream infections with paired microbiome data indicates that bacteria may translocate from the gut into the systemic circulation of COVID-19 patients. These results are consistent with a direct role for gut microbiome dysbiosis in enabling dangerous secondary infections during COVID-19
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