700 research outputs found

    The F&ST experience : a narrative study

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    The purpose of this qualitative research, framed as a narrative inquiry, was to explore the experiences of a select family’s participation in the Family and Schools Together (F&ST) program at an elementary school in Northwestern Saskatchewan. All members of this select family were Caucasian and of non-aboriginal descent. These participating family members, a mother, father and their three boys, told their story within the context of guided questions in the setting of individual unstructured interviews. The interviews were audio taped, transcribed, analyzed for unique and common threads and written into the form of a family narrative. Although unique threads were discovered from the analysis, the following common experiences emerged: the importance of taking time for family, the benefit of connecting with others and building relationships, the perception of the goals behind F&ST and favourite activities. These experiences were incorporated into the family narrative. This study offers the opportunity for a greater awareness into the impact, participation in the F&ST (Family and Schools Together) intervention program has had on one select family and how that impact can be used to strengthen the delivery of that program and encourage others to get involved. Findings from this study show that the select family in this study experienced positive growth in family relationships, and positive affiliation with their school and community as a result of participating in F&ST. The findings from this study form the basis for implications for practice as well as for areas of further research

    Metallurgical Structures of As-Cast and Heat-Treated High-Palladium Dental Alloys

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    Scanning electron microscope observations and energy-dispersive spectroscopic analyses have been performed on two first-generation and two second-generation high-palladium dental casting alloys. A specimen design simulating a maxillary central incisor coping was employed to conserve metal, while providing thin and thick sections to yield a range of solidification rates. The alloys were centrifugally cast in air, following standard dental laboratory techniques; three castings were prepared for each alloy. Each casting was sectioned to produce two mirror-image specimens, and one specimen received the appropriate oxidation heat treatment, followed by a simulated full porcelain firing sequence. After metallographic polishing, specimens were examined with a scanning electron microscope. The as-cast alloys displayed multi-phase microstructures which could be explained by the rapid solidification conditions and the relevant phase diagrams. The simulated porcelain firing heat treatment caused a variety of bulk microstructural changes in the coping sections, along with formation of complex subsurface oxidation regions which were less thick for the second-generation alloys. Elemental compositions of the palladium solid solution matrix in the heat-treated alloys were in good agreement with nominal alloy compositions provided by the manufacturers. Ruthenium-rich particles found in the microstructures of three alloys are consistent with a proposed mechanism for grain refinement

    Metallurgical Structures of As-Cast and Heat-Treated High-Palladium Dental Alloys

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    Scanning electron microscope observations and energy-dispersive spectroscopic analyses have been performed on two first-generation and two second-generation high-palladium dental casting alloys. A specimen design simulating a maxillary central incisor coping was employed to conserve metal, while providing thin and thick sections to yield a range of solidification rates. The alloys were centrifugally cast in air, following standard dental laboratory techniques; three castings were prepared for each alloy. Each casting was sectioned to produce two mirror-image specimens, and one specimen received the appropriate oxidation heat treatment, followed by a simulated full porcelain firing sequence. After metallographic polishing, specimens were examined with a scanning electron microscope. The as-cast alloys displayed multi-phase microstructures which could be explained by the rapid solidification conditions and the relevant phase diagrams. The simulated porcelain firing heat treatment caused a variety of bulk microstructural changes in the coping sections, along with formation of complex subsurface oxidation regions which were less thick for the second-generation alloys. Elemental compositions of the palladium solid solution matrix in the heat-treated alloys were in good agreement with nominal alloy compositions provided by the manufacturers. Ruthenium-rich particles found in the microstructures of three alloys are consistent with a proposed mechanism for grain refinement

    Room Temperature Aging of Pd-Cu-Ga Dental Alloys

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    Specimens of three Pd-Cu-Ga dental alloys cast five years ago and subsequently stored at room temperature were reexamined and observed to have lower amounts of the eutectic constituents in the near-surface region than originally present, along with other microstructural changes. This previously unreported room temperature aging behavior of these alloys is attributed to the presence of high-diffusivity paths in the non-equilibrium ascast eutectic structures and to the essential role of the surface for the vacancy diffusion mechanism. These results may have important clinical significance for the ill vivo corrosion resistance and long-term biocompatibility of the Pd-Cu-Ga alloys

    Inducing and exploiting activation sparsity for fast neural network inference

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    Optimizing convolutional neural networks for fast inference has recently become an extremely active area of research. One of the go-to solutions in this context is weight pruning, which aims to reduce computational and memory footprint by removing large subsets of the connections in a neural network. Surprisingly, much less attention has been given to exploiting sparsity in the activation maps, which tend to be naturally sparse in many settings thanks to the structure of rectified linear (ReLU) activation functions. In this paper, we present an in-depth analysis of methods for maximizing the sparsity of the activations in a trained neural network, and show that, when coupled with an efficient sparse-input convolution algorithm, we can leverage this sparsity for significant performance gains. To induce highly sparse activation maps without accuracy loss, we introduce a new regularization technique, coupled with a new threshold-based sparsification method based on a parameterized activation function called Forced-Activation-Threshold Rectified Linear Unit (FATReLU). We examine the impact of our methods on popular image classification models, showing that most architectures can adapt to significantly sparser activation maps without any accuracy loss. Our second contribution is showing that these these compression gains can be translated into inference speedups: we provide a new algorithm to enable fast convolution operations over networks with sparse activations, and show that it can enable significant speedups for end-to-end inference on a range of popular models on the large-scale ImageNet image classification task on modern Intel CPUs, with little or no retraining cost

    ICP0 antagonizes Stat 1-dependent repression of herpes simplex virus: implications for the regulation of viral latency

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    BACKGROUND: The herpes simplex virus type 1 (HSV-1) ICP0 protein is an E3 ubiquitin ligase, which is encoded within the HSV-1 latency-associated locus. When ICP0 is not synthesized, the HSV-1 genome is acutely susceptible to cellular repression. Reciprocally, when ICP0 is synthesized, viral replication is efficiently initiated from virions or latent HSV-1 genomes. The current study was initiated to determine if ICP0's putative role as a viral interferon (IFN) antagonist may be relevant to the process by which ICP0 influences the balance between productive replication versus cellular repression of HSV-1. RESULTS: Wild-type (ICP0(+)) strains of HSV-1 produced lethal infections in scid or rag2(-/- )mice. The replication of ICP0(- )null viruses was rapidly repressed by the innate host response of scid or rag2(-/- )mice, and the infected animals remained healthy for months. In contrast, rag2(-/- )mice that lacked the IFN-α/β receptor (rag2(-/- )ifnar(-/-)) or Stat 1 (rag2(-/- )stat1(-/-)) failed to repress ICP0(- )viral replication, resulting in uncontrolled viral spread and death. Thus, the replication of ICP0(- )viruses is potently repressed in vivo by an innate immune response that is dependent on the IFN-α/β receptor and the downstream transcription factor, Stat 1. CONCLUSION: ICP0's function as a viral IFN antagonist is necessary in vivo to prevent an innate, Stat 1-dependent host response from rapidly repressing productive HSV-1 replication. This antagonistic relationship between ICP0 and the host IFN response may be relevant in regulating whether the HSV-1 genome is expressed, or silenced, in virus-infected cells in vivo. These results may also be clinically relevant. IFN-sensitive ICP0(- )viruses are avirulent, establish long-term latent infections, and induce an adaptive immune response that is highly protective against lethal challenge with HSV-1. Therefore, ICP0(- )viruses appear to possess the desired safety and efficacy profile of a live vaccine against herpetic disease

    Genome-scale analysis identifies paralog lethality as a vulnerability of chromosome 1p loss in cancer.

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    Functional redundancy shared by paralog genes may afford protection against genetic perturbations, but it can also result in genetic vulnerabilities due to mutual interdependency1-5. Here, we surveyed genome-scale short hairpin RNA and CRISPR screening data on hundreds of cancer cell lines and identified MAGOH and MAGOHB, core members of the splicing-dependent exon junction complex, as top-ranked paralog dependencies6-8. MAGOHB is the top gene dependency in cells with hemizygous MAGOH deletion, a pervasive genetic event that frequently occurs due to chromosome 1p loss. Inhibition of MAGOHB in a MAGOH-deleted context compromises viability by globally perturbing alternative splicing and RNA surveillance. Dependency on IPO13, an importin-β receptor that mediates nuclear import of the MAGOH/B-Y14 heterodimer9, is highly correlated with dependency on both MAGOH and MAGOHB. Both MAGOHB and IPO13 represent dependencies in murine xenografts with hemizygous MAGOH deletion. Our results identify MAGOH and MAGOHB as reciprocal paralog dependencies across cancer types and suggest a rationale for targeting the MAGOHB-IPO13 axis in cancers with chromosome 1p deletion

    SMAC mimetics promote NIK-dependent inhibition of CD4+ TH17 cell differentiation

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    Second mitochondria-derived activator of caspase (SMAC) mimetics (SMs) are selective antagonists of the inhibitor of apoptosis proteins (IAPs), which activate noncanonical NF-κB signaling and promote tumor cell death. Through gene expression analysis, we found that treatment of CD4+ T cells with SMs during T helper 17 (TH17) cell differentiation disrupted the balance between two antagonistic transcription factor modules. Moreover, proteomics analysis revealed that SMs altered the abundance of proteins associated with cell cycle, mitochondrial activity, and the balance between canonical and noncanonical NF-κB signaling. Whereas SMs inhibited interleukin-17 (IL-17) production and ameliorated TH17 cell–driven inflammation, they stimulated IL-22 secretion. Mechanistically, SM-mediated activation of NF-κB–inducing kinase (NIK) and the transcription factors RelB and p52 directly suppressed Il17a expression and IL-17A protein production, as well as the expression of a number of other immune genes. Induction of IL-22 production correlated with the NIK-dependent reduction in cMAF protein abundance and the enhanced activity of the aryl hydrocarbon receptor. Last, SMs also increased IL-9 and IL-13 production and, under competing conditions, favored the differentiation of naïve CD4+ T cells into TH2 cells rather than TH17 cells. These results demonstrate that SMs shape the gene expression and protein profiles of TH17 cells and inhibit TH17 cell–driven autoimmunity

    The detection of experimental myocardial infarcts by photoscanning : A preliminary report

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/32339/1/0000409.pd
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