3,350 research outputs found

    Resist Performance Using Spectroscopic Ellipsometry

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    The technique of spectroscopic ellipsometry was employed to study the effects of residual solvents in chemically amplified photoresists on the dissolution characteristics and optical constants of the spin-cast film. Ellipsometric measurements were made for resist films with no bake, with soft bakes, and with both soft bakes and post-exposure bakes, at various baking temperatures. Exposures of these films were performed using a KrF excimer laser (248 nm) with a beam splitter lens element to increase the exposure area. To increase the accuracy of the experimental data, measurements were made at three different angles over a sampling wavelength range of 200 nm to 800 nm. Resist thickness and optical parameters (n and k) were extracted by fitting the experimental data to a theoretical model

    Decoding the multifaceted HIV-1 virus-host interactome

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    Recently in BMC Medical Genomics, Tozeren and colleagues have uncovered virus-host interactions by searching for conserved peptide motifs in HIV and human proteins. Their computational model provides a novel perspective in the interpretation of high-throughput data on the HIV-host interactome

    IL-33 ameliorates Alzheimer’s disease-like pathology and cognitive decline

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    Alzheimer’s disease (AD) is a devastating condition with no known effective treatment. AD is characterized by memory loss as well as impaired locomotor ability, reasoning, and judgment. Emerging evidence suggests that the innate immune response plays a major role in the pathogenesis of AD. In AD, the accumulation of β-amyloid (Aβ) in the brain perturbs physiological functions of the brain, including synaptic and neuronal dysfunction, microglial activation, and neuronal loss. Serum levels of soluble ST2 (sST2), a decoy receptor for interleukin (IL)-33, increase in patients with mild cognitive impairment, suggesting that impaired IL-33/ST2 signaling may contribute to the pathogenesis of AD. Therefore, we investigated the potential therapeutic role of IL-33 in AD, using transgenic mouse models. Here we report that IL-33 administration reverses synaptic plasticity impairment and memory deficits in APP/PS1 mice. IL-33 administration reduces soluble Aβ levels and amyloid plaque deposition by promoting the recruitment and Aβ phagocytic activity of microglia; this is mediated by ST2/p38 signaling activation. Furthermore, IL-33 injection modulates the innate immune response by polarizing microglia/macrophages toward an antiinflammatory phenotype and reducing the expression of proinflammatory genes, including IL-1β, IL-6, and NLRP3, in the cortices of APP/PS1 mice. Collectively, our results demonstrate a potential therapeutic role for IL-33 in AD

    Secretome Analysis of Skeletal Myogenesis Using SILAC and Shotgun Proteomics

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    Myogenesis, the formation of skeletal muscle, is a multistep event that commences with myoblast proliferation, followed by cell-cycle arrest, and finally the formation of multinucleated myotubes via fusion of mononucleated myoblasts. Each step is orchestrated by well-documented intracellular factors, such as cytoplasmic signalling molecules and nuclear transcription factors. Regardless, the key step in getting a more comprehensive understanding of the regulation of myogenesis is to explore the extracellular factors that are capable of eliciting the downstream intracellular factors. This could further provide valuable insight into the acute cellular response to extrinsic cues in maintaining normal muscle development. In this paper, we survey the intracellular factors that respond to extracellular cues that are responsible for the cascades of events during myogenesis: myoblast proliferation, cell-cycle arrest of myoblasts, and differentiation of myoblasts into myotubes. This focus on extracellular perspective of muscle development illustrates our mass spectrometry-based proteomic approaches to identify differentially expressed secreted factors during skeletal myogenesis

    Long-term evaluation of cantilevered versus fixed–fixed resin-bonded fixed partial dentures for missing maxillary incisors

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    © 2016 Elsevier LtdObjectives To evaluate the long-term longevity and patient-reported outcomes of two-unit cantilevered (CL2) and three-unit fixed–fixed (FF3) resin-bonded fixed partial dentures (RBFPDs) for the replacement of a maxillary permanent incisor. Materials and methods Twenty-eight subjects were randomly assigned to receive either a CL2 or FF3 RBFPD placed by one operator. Prosthesis longevity was determined by clinical examination and history. Success was defined as absence of complications requiring intervention and survival as retention of the original prosthesis in mouth. Subjects’ satisfaction was assessed using visual analogue scale (VAS) and oral health-related quality of life (OHRQoL) using Oral Health Impact Profile (OHIP-49). Outcomes were analysed with t-test/Mann–Whitney U test, chi-square and log-rank test at significance level α = 0.05. Results Twenty-two subjects were reviewed. Thirteen of fifteen CL2 and ten of fourteen FF3 RBFPDs were examined (79.3 percent response rate) with a mean service life of 216.5 ± 20.8 months. All CL2 RBFPDs survived with no complications while only 10 percent of FF3 experienced no complications and only 50 percent of them survived (both P = 0.000). CL2 had a significantly better success and survival rate than FF3 (P = 0.000 and P = 0.009, respectively). There was no significant difference in subjects’ satisfaction and OHRQoL apart from CL2 group subjects had a higher satisfaction in cleaning of the prosthesis (84.1 ± 13.6) than FF3 group (72.6 ± 11.7) (P = 0.05). Conclusions Two-unit cantilevered RBFPDs were observed to have a significantly better success and survival than the FF3 design for the replacement of a maxillary incisor. Good patient-reported outcomes have been found for RBFPDs in single-tooth replacement in aesthetic zone.postprin

    Tropism of and Innate Immune Responses to the Novel Human Betacoronavirus Lineage C Virus in Human Ex Vivo Respiratory Organ Cultures

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    Since April 2012, there have been 17 laboratory-confirmed human cases of respiratory disease associated with newly recognized human betacoronavirus lineage C virus EMC (HCoV-EMC), and 7 of them were fatal. The transmissibility and pathogenesis of HCoV-EMC remain poorly understood, and elucidating its cellular tropism in human respiratory tissues will provide mechanistic insights into the key cellular targets for virus propagation and spread. We utilized ex vivo cultures of human bronchial and lung tissue specimens to investigate the tissue tropism and virus replication kinetics following experimental infection with HCoV-EMC compared with those following infection with human coronavirus 229E (HCoV-229E) and severe acute respiratory syndrome coronavirus (SARS-CoV). The innate immune responses elicited by HCoV-EMC were also investigated. HCoV-EMC productively replicated in human bronchial and lung ex vivo organ cultures. While SARS-CoV productively replicated in lung tissue, replication in human bronchial tissue was limited. Immunohistochemistry revealed that HCoV-EMC infected nonciliated bronchial epithelium, bronchiolar epithelial cells, alveolar epithelial cells, and endothelial cells. Transmission electron microscopy showed virions within the cytoplasm of bronchial epithelial cells and budding virions from alveolar epithelial cells (type II). In contrast, there was minimal HCoV-229E infection in these tissues. HCoV-EMC failed to elicit strong type I or III interferon (IFN) or proinflammatory innate immune responses in ex vivo respiratory tissue cultures. Treatment of human lung tissue ex vivo organ cultures with type I IFNs (alpha and beta IFNs) at 1 h postinfection reduced the replication of HCoV-EMC, suggesting a potential therapeutic use of IFNs for treatment of human infection

    Phase Diagram and Magnetocaloric Effects in Aluminum Doped MnNiGe Alloys

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    The magnetocaloric and thermomagnetic properties of the MnNiGe1-xAlx system have been studied by temperature- dependent x- ray diffraction, differential scanning calorimetry (DSC), and magnetization measurements. The partial substitution of Al for Ge in MnNiGe1-xAlx results in a first order magnetostructural transition (MST) from a hexagonal ferromagnetic to an orthorhombic antiferromagnetic phase at 186K (for x 0.09). A large magnetic entropy change of Delta SM = - 17.6 J/kg K for DeltaH = 5T was observed in the vicinity of TM 186K for x 0.09. The value is comparable to those of giant magnetocaloric materials such as Gd5Si2Ge2, MnFeP0.45As0.55, and Ni50Mn37Sn13. The values of the latent heat (L 6.6 J/g) and corresponding total entropy changes (DeltaST 35 J/kg K) have been evaluated for the MST using DSC measurements. Large negative values of Delta SM of - 5.8 and - 4.8 J/kg K for DeltaH = 5T in the vicinity of TC were observed for x 0.09 and 0.085, respectively. A concentration- dependent phase diagram of transition temperatures (magnetic, structural, and magnetostructural) has been generated using magnetic, XRD, and DSC data. The role of magnetic and structural changes on transition temperatures is discussed

    Strategic Employee Scheduling

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    Abstract. Today's highly competitive economy calls for new methods of management. Advanced practices have been proposed to manage human resources, often acclaimed to be the most important assets of any organisation. However, computer models and applications to support these methods are often not available, or not until it is much too late. This paper presents several directions for advances in strategic employee scheduling, as well as our approach for implementing these concepts

    Hedgehog pathway dysregulation contributes to the pathogenesis of human gastrointestinal stromal tumors via GLI-mediated activation of KIT expression.

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    Gastrointestinal stromal tumors (GIST) arise within the interstitial cell of Cajal (ICC) lineage due to activating KIT/PDGFRA mutations. Both ICC and GIST possess primary cilia (PC), which coordinate PDGFRA and Hedgehog signaling, regulators of gastrointestinal mesenchymal development. Therefore, we hypothesized that Hedgehog signaling may be altered in human GIST and controls KIT expression. Quantitative RT-PCR, microarrays, and next generation sequencing were used to describe Hedgehog/PC-related genes in purified human ICC and GIST. Genetic and pharmacologic approaches were employed to investigate the effects of GLI manipulation on KIT expression and GIST cell viability. We report that Hedgehog pathway and PC components are expressed in ICC and GIST and subject to dysregulation during GIST oncogenesis, irrespective of KIT/PDGFRA mutation status. Using genomic profiling, 10.2% of 186 GIST studied had potentially deleterious genomic alterations in 5 Hedgehog-related genes analyzed, including in the PTCH1 tumor suppressor (1.6%). Expression of the predominantly repressive GLI isoform, GLI3, was inversely correlated with KIT mRNA levels in GIST cells and non-KIT/non-PDGFRA mutant GIST. Overexpression of the 83-kDa repressive form of GLI3 or small interfering RNA-mediated knockdown of the activating isoforms GLI1/2 reduced KIT mRNA. Treatment with GLI1/2 inhibitors, including arsenic trioxide, significantly increased GLI3 binding to the KIT promoter, decreased KIT expression, and reduced viability in imatinib-sensitive and imatinib-resistant GIST cells. These data offer new evidence that genes necessary for Hedgehog signaling and PC function in ICC are dysregulated in GIST. Hedgehog signaling activates KIT expression irrespective of mutation status, offering a novel approach to treat imatinib-resistant GIST
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