830 research outputs found

    Maximum-likelihood Localization of Overlapping Point Sources in 3D Microscopy Using CLEAN

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    Precise 3D point localization is increasingly important in microscopy, but algorithms break down when PSFs overlap. We adapt the CLEAN algorithm from astronomical imaging to enable MLE localization of high-density datasets

    MHC antigens in interferon γ (IFNγ) receptor deficient mice: IFNγ-independent up-regulation of MHC class II in renal tubules

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    MHC antigens in interferon γ (IFNγ) receptor deficient mice: IFNγ-independent up-regulation of MHC class II in renal tubules. MHC class II gene products in parenchymal cells, such as tubular epithelial cells in kidney, may play a role in the regulation of autoimmune reactions. Expression of MHC class II in renal tubular cells is normally very low, but it increases considerably under various pathologic conditions. The predominant role of IFNγ in up-regulation of MHC class II expression has been demonstrated repeatedly. We tested the existence of alternative pathways of MHC class II regulation using IFNγ receptor-deficient (IFNγR-/-) mice. Mutant and wild type mice received 50 µg bacterial endotoxin (LPS) i.p. Four days later the kidneys were removed for immunofluorescence examination. In agreement with published results LPS provoked an increase of immunoreactivity for MHC class I and MHC class II in proximal tubules of wild type mice. While MHC class I up-regulation was strictly IFNγ receptor-dependent, up-regulation of MHC II was still evident in mutant mice, although less than in wild type mice. Since injection of IFNγ induced proximal tubular MHC class II expression in wild type mice but not in IFNγR-/- mice, an alternative signaling pathway for IFNγ does not seem to exist. Thus, up-regulation of MHC class II expression in renal tubules does not necessarily require IFNγ. The markedly patchy pattern of immunofluorescence in IFNγR-/- mice suggests that induction of MHC class II after LPS injection may represent renal injury due to shock

    Optical Imaging Using Binary Sensors

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    This paper addresses the problem of reconstructing an image from 1-bit-quantized measurements, considering a simple but nonconventional optical acquisition model. Following a compressed-sensing design, a known pseudo-random phase-shifting mask is introduced at the aperture of the optical system. The associated reconstruction algorithm is tailored to this mask. Our results demonstrate the feasibility of the whole approach for reconstructing grayscale images

    The fusion protein SS18-SSX1 employs core Wnt pathway transcription factors to induce a partial Wnt signature in synovial sarcoma.

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    Expression of the SS18/SYT-SSX fusion protein is believed to underlie the pathogenesis of synovial sarcoma (SS). Recent evidence suggests that deregulation of the Wnt pathway may play an important role in SS but the mechanisms whereby SS18-SSX might affect Wnt signaling remain to be elucidated. Here, we show that SS18/SSX tightly regulates the elevated expression of the key Wnt target AXIN2 in primary SS. SS18-SSX is shown to interact with TCF/LEF, TLE and HDAC but not β-catenin in vivo and to induce Wnt target gene expression by forming a complex containing promoter-bound TCF/LEF and HDAC but lacking β-catenin. Our observations provide a tumor-specific mechanistic basis for Wnt target gene induction in SS that can occur in the absence of Wnt ligand stimulation

    The effects of death and post-mortem cold ischemia on human tissue transcriptomes

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    Post-mortem tissues samples are a key resource for investigating patterns of gene expression. However, the processes triggered by death and the post-mortem interval (PMI) can significantly alter physiologically normal RNA levels. We investigate the impact of PMI on gene expression using data from multiple tissues of post-mortem donors obtained from the GTEx project. We find that many genes change expression over relatively short PMIs in a tissue-specific manner, but this potentially confounding effect in a biological analysis can be minimized by taking into account appropriate covariates. By comparing ante- and post-mortem blood samples, we identify the cascade of transcriptional events triggered by death of the organism. These events do not appear to simply reflect stochastic variation resulting from mRNA degradation, but active and ongoing regulation of transcription. Finally, we develop a model to predict the time since death from the analysis of the transcriptome of a few readily accessible tissues.Peer ReviewedPostprint (published version
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