511 research outputs found

    Library Buildings And The Building Of A Collaborative Research Collection At The Tri-College Library Consortium

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    This report is the product of a planning grant awarded by The Andrew W. Mellon Foundation in 2001 to the Tri-College Library Consortium, which comprises the libraries of Bryn Mawr, Haverford and Swarthmore Colleges. The grant proposal, entitled “Library Buildings and the Building of a Collaborative Research Collection at the Tri-Colleges,” set out a research agenda designed to address two central questions. The first question was a challenge: How could the three libraries come to terms with space problems caused by ever-growing collections and increasing demands to accommodate media, teaching, and student study areas in an environment in which library building expansion was a remote possibility? The second question was an opportunity: Could the libraries take advantage of their history of cooperation and the powerful tool of a unified online catalog to create a single research-quality collection out of the combined holdings of three strong liberal arts colleges? Working with a consultant, a seven-member Planning Group representing the three colleges and the consortium gathered data on the collections, convened focus groups of faculty and students, and engaged three publishing industry experts to assess the state of electronic publishing. After analyzing the data, the Planning Group studied alternatives for maximizing collection space and made recommendations for new models and strategies to be pursued by the Tri-Colleges consortium

    Inhibition of IFN-γ Signaling by an Epstein-Barr Virus Immediate-Early Protein

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    AbstractViruses have evolved elaborate mechanisms to target many aspects of the host's immune response. The cytokine IFN-γ plays a central role in resistance of the host to infection via direct antiviral effects as well as modulation of the immune response. In this study, we demonstrate that the Epstein-Barr virus (EBV) immediate-early protein, BZLF1, inhibits the IFN-γ signaling pathway. BZLF1 decreases the ability of IFN-γ to activate a variety of important downstream target genes, such as IRF-1, p48, and CIITA, and prevents IFN-γ-induced class II MHC surface expression. Additionally, BZLF1 inhibits IFN-γ-induced STAT1 tyrosine phosphorylation and nuclear translocation. Finally, we demonstrate that BZLF1 decreases expression of the IFN-γ receptor, suggesting a mechanism by which EBV may escape antiviral immune responses during primary infection

    Evidence for lateral transfer of genes encoding ferredoxins, nitroreductases, NADH oxidase, and alcohol dehydrogenase 3 from anaerobic prokaryotes to Giardia lamblia and Entamoeba histolytica

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    Author Posting. © American Society for Microbiology, 2002. This article is posted here by permission of American Society for Microbiology for personal use, not for redistribution. The definitive version was published in Eukaryotic Cell 1 (2002): 181-190, doi:10.1128/EC.1.2.181-190.2002.Giardia lamblia and Entamoeba histolytica are amitochondriate, microaerophilic protists which use fermentation enzymes like those of bacteria to survive anaerobic conditions within the intestinal lumen. Genes encoding fermentation enzymes and related electron transport peptides (e.g., ferredoxins) in giardia organisms and amebae are hypothesized to be derived from either an ancient anaerobic eukaryote (amitochondriate fossil hypothesis), a mitochondrial endosymbiont (hydrogen hypothesis), or anaerobic bacteria (lateral transfer hypothesis). The goals here were to complete the molecular characterization of giardial and amebic fermentation enzymes and to determine the origins of the genes encoding them, when possible. A putative giardia [2Fe-2S]ferredoxin which had a hypothetical organelle-targeting sequence at its N terminus showed similarity to mitochondrial ferredoxins and the hydrogenosomal ferredoxin of Trichomonas vaginalis (another luminal protist). However, phylogenetic trees were star shaped, with weak bootstrap support, so we were unable to confirm or rule out the endosymbiotic origin of the giardia [2Fe-2S]ferredoxin gene. Putative giardial and amebic 6-kDa ferredoxins, ferredoxin-nitroreductase fusion proteins, and oxygen-insensitive nitroreductases each tentatively supported the lateral transfer hypothesis. Although there were not enough sequences to perform meaningful phylogenetic analyses, the unique common occurrence of these peptides and enzymes in giardia organisms, amebae, and the few anaerobic prokaryotes suggests the possibility of lateral transfer. In contrast, there was more robust phylogenetic evidence for the lateral transfer of G. lamblia genes encoding an NADH oxidase from a gram-positive coccus and a microbial group 3 alcohol dehydrogenase from thermoanaerobic prokaryotes. In further support of lateral transfer, the G. lamblia NADH oxidase and adh3 genes appeared to have an evolutionary history distinct from those of E. histolytica.This work was supported by NIH grants (AI33492 to J.S., AI43273 to M.L.S., and AI46516 to B.J.L.). Additional support was provided by the G. Unger Vetlesen Foundation and LI-COR Biotechnology

    The Past, Present and Future of Sleep Measurement in Mild Cognitive Impairment and Early Dementia – Towards a Core Outcome Set:A Scoping Review

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    STUDY OBJECTIVES: Sleep abnormalities emerge early in dementia and may accelerate cognitive decline. Their accurate characterization may facilitate earlier clinical identification of dementia and allow for assessment of sleep intervention efficacy. This scoping review determines how sleep is currently measured and reported in Mild Cognitive Impairment (MCI) and early dementia, as a basis for future core outcome alignment. METHODS: This review follows the PRISMA Guidelines for Scoping Reviews. CINAHL, Embase, Medline, Psychinfo, and British Nursing Index databases were searched from inception—March 12, 2021. Included studies had participants diagnosed with MCI and early dementia and reported on sleep as a key objective/ outcome measure. RESULTS: Nineteen thousand five hundred and ninety-six titles were returned following duplicate removal with 188 studies [N] included in final analysis. Sleep data was reported on 17 139 unique, diagnostically diverse participants (n). “Unspecified MCI” was the most common diagnosis amongst patients with MCI (n = 5003, 60.6%). Despite technological advances, sleep was measured most commonly by validated questionnaires (n = 12 586, N = 131). Fewer participants underwent polysomnography (PSG) (n = 3492, N = 88) and actigraphy (n = 3359, N = 38) with little adoption of non-PSG electroencephalograms (EEG) (n = 74, N = 3). Sleep outcome parameters were reported heterogeneously. 62/165 (37.6%) were described only once in the literature (33/60 (60%) in interventional studies). There was underrepresentation of circadian (n = 725, N = 25) and micro-architectural (n = 360, N = 12) sleep parameters. CONCLUSIONS: Alongside under-researched areas, there is a need for more detailed diagnostic characterization. Due to outcome heterogeneity, we advocate for international consensus on core sleep outcome parameters to support causal inference and comparison of therapeutic sleep interventions

    NMDA Receptors Subserve Persistent Neuronal Firing during Working Memory in Dorsolateral Prefrontal Cortex

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    SummaryNeurons in the primate dorsolateral prefrontal cortex (dlPFC) generate persistent firing in the absence of sensory stimulation, the foundation of mental representation. Persistent firing arises from recurrent excitation within a network of pyramidal Delay cells. Here, we examined glutamate receptor influences underlying persistent firing in primate dlPFC during a spatial working memory task. Computational models predicted dependence on NMDA receptor (NMDAR) NR2B stimulation, and Delay cell persistent firing was abolished by local NR2B NMDAR blockade or by systemic ketamine administration. AMPA receptors (AMPARs) contributed background depolarization to sustain network firing. In contrast, many Response cells were sensitive to AMPAR blockade and increased firing after systemic ketamine, indicating that models of ketamine actions should be refined to reflect neuronal heterogeneity. The reliance of Delay cells on NMDAR may explain why insults to NMDARs in schizophrenia or Alzheimer’s disease profoundly impair cognition

    A longitudinal study of Sin Nombre virus prevalence in rodents, southeastern Arizona.

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    We determined the prevalence of Sin Nombre virus antibodies in small mammals in southeastern Arizona. Of 1,234 rodents (from 13 species) captured each month from May through December 1995, only mice in the genus Peromyscus were seropositive. Antibody prevalence was 14.3% in 21 white-footed mice (P. leucopus), 13.3% in 98 brush mice (P. boylii), 0.8% in 118 cactus mice (P. eremicus), and 0% in 2 deer mice (P. maniculatus). Most antibody-positive mice were adult male Peromyscus captured close to one another early in the study. Population dynamics of brush mice suggest a correlation between population size and hantavirus-antibody prevalence

    Effects of Acceptance and Commitment Therapy on Impulsive Decision Making

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    This study examined the transdiagnostic effect of acceptance and commitment therapy (ACT) on impulsive decision making in a community sample. Forty adults were randomized to eight individual sessions of ACT or an inactive control. Participants completed pre-, mid-, and post-assessments for psychological symptoms, overall behavior change, valued living, delay discounting, psychological flexibility, and distress tolerance. Data were analyzed with multilevel modeling of growth curves. Significant interaction effects of time and condition were observed for psychological flexibility, distress tolerance, psychological symptoms, and the obstruction subscale of valued living. No significant interaction effect was found for two delay discounting tasks nor the progress subscale of valued living. The ACT condition had a significantly larger reduction of problem behavior at post-assessment. The results support use of ACT as a transdiagnostic treatment for impulsive behaviors. The lack of change in delay discounting contrasts previous research
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