44 research outputs found

    Retrieval of Brain Tumors with Region-Specific Bag-of-Visual-Words Representations in Contrast-Enhanced MRI Images

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    A content-based image retrieval (CBIR) system is proposed for the retrieval of T1-weighted contrast-enhanced MRI (CE-MRI) images of brain tumors. In this CBIR system, spatial information in the bag-of-visual-words model and domain knowledge on the brain tumor images are considered for the representation of brain tumor images. A similarity metric is learned through a distance metric learning algorithm to reduce the gap between the visual features and the semantic concepts in an image. The learned similarity metric is then used to measure the similarity between two images and then retrieve the most similar images in the dataset when a query image is submitted to the CBIR system. The retrieval performance of the proposed method is evaluated on a brain CE-MRI dataset with three types of brain tumors (i.e., meningioma, glioma, and pituitary tumor). The experimental results demonstrate that the mean average precision values of the proposed method range from 90.4% to 91.5% for different views (transverse, coronal, and sagittal) with an average value of 91.0%

    Content-based image retrieval using spatial layout information in brain tumor T1-weighted contrast-enhanced MR images.

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    This study aims to develop content-based image retrieval (CBIR) system for the retrieval of T1-weighted contrast-enhanced MR (CE-MR) images of brain tumors. When a tumor region is fed to the CBIR system as a query, the system attempts to retrieve tumors of the same pathological category. The bag-of-visual-words (BoVW) model with partition learning is incorporated into the system to extract informative features for representing the image contents. Furthermore, a distance metric learning algorithm called the Rank Error-based Metric Learning (REML) is proposed to reduce the semantic gap between low-level visual features and high-level semantic concepts. The effectiveness of the proposed method is evaluated on a brain T1-weighted CE-MR dataset with three types of brain tumors (i.e., meningioma, glioma, and pituitary tumor). Using the BoVW model with partition learning, the mean average precision (mAP) of retrieval increases beyond 4.6% with the learned distance metrics compared with the spatial pyramid BoVW method. The distance metric learned by REML significantly outperforms three other existing distance metric learning methods in terms of mAP. The mAP of the CBIR system is as high as 91.8% using the proposed method, and the precision can reach 93.1% when the top 10 images are returned by the system. These preliminary results demonstrate that the proposed method is effective and feasible for the retrieval of brain tumors in T1-weighted CE-MR Images

    LPS-induced decrease in intracellular labile zinc, [Zn]i, contributes to apoptosis in cultured sheep pulmonary artery endothelial cells

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    A role in signal transduction for a vanishingly small labile pool of intracellular zinc ([Zn]i) has been inferred by the sensitivity of various physiological pathways to zinc chelators such as N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) and/or associations with changes in nonprotein-bound zinc-sensitive fluorophores. Although we (44) reported that LPS-induced apoptosis in cultured sheep pulmonary artery endothelial cells (SPAEC) was exacerbated by TPEN, 1) we did not detect acute (30 min) changes in [Zn]i, and 2) it is unclear from other reports whether LPS increases or decreases [Zn]i and whether elevations or decreases in [Zn]i are associated with cell death and/or apoptosis. In the present study, we used both chemical (FluoZin-3 via live cell epifluorescence microscopy and fluorescence-activated cell sorting) and genetic (luciferase activity of a chimeric reporter encoding zinc-sensitive metal-response element and changes in steady-state mRNA of zinc importer, SLC39A14 or ZIP14) techniques to show that LPS caused a delayed time-dependent (2–4 h) decrease in [Zn]i in SPAEC. A contributory role of decreases in [Zn]i in LPS-induced apoptosis (as determined by caspase-3/7 activation, annexin-V binding, and cytochrome c release) in SPAECs was revealed by mimicking the effect of LPS with the zinc chelator, TPEN, and inhibiting LPS- (or TPEN)-induced apoptosis with exogenous zinc. Collectively, these are the first data demonstrating a signaling role for decrease in [Zn]i in pulmonary endothelial cells and suggest that endogenous levels of labile zinc may affect sensitivity of pulmonary endothelium to the important and complex proapoptotic stimulus of LPS

    Externalization of Cardiolipin as an “Eat-Me” Mitophageal Signal is Facilitated by NDPK-D

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    International audienceMitochondria are vulnerable to damage, particularly by oxidative stress-induced injury imposed by many genetic and environmental factors. These malfunctioning mitochondria have to be eliminated to prevent an increasing generation of reactive oxygen species (ROS) that could trigger cell injury and death. This selective elimination of damaged mitochondria is executed via initiation of a specific type of mitochondrial autophagy - mitophagy. Our previous work has established that a mitochondria-specific phospholipid, cardiolipin (CL) - normally asymmetrically distributed between the mitochondrial inner (IMM) and outer (OMM) membranes - undergoes translocation to the OMM where it becomes externalized to the mitochondrial surface. This externalized CL serves as recognition signal for the autophageal machinery leading to the elimination of these mitochondria. The recognition is achieved through the selective binding of externalized CL with microtubule-associated protein light chain 3 (LC3). The mechanisms driving CL redistribution/externalization remain unknown. By using LC-MS analysis of mono-lyso-cardiolipins (mL-CL) formed by phospholipase A2 exogenously added and impermeable to mitochondria, we established that treatment of HeLa cells with a protonophoric uncoupler, CCCP, triggers mitophagy of depolarized mitochondria accompanied by CL externalization. We further found that CL externalization is dependent on an intermembrane space enzyme, nucleoside diphosphate kinase, NDPK-D. The latter, upon interaction with CL, loses its kinase function and turns into a CL-translocase. CL externalization and mitophagy were stimulated by transfecting HeLa cells with w/type but not mutant R90A NDPK-D, incapable of CL binding. Identification of NDPK-D as a pro-mitophageal CL translocase may be used in drug discovery paradigms for regulation of “mitochondrial health.

    Unusual Peroxidase Activity of Polynitroxylated Pegylated Hemoglobin: Elimination of H\u3csub\u3e2\u3c/sub\u3eO\u3csub\u3e2\u3c/sub\u3e Coupled with Intramolecular Oxidation of Nitroxides

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    Polynitroxylated hemoglobin (Hb(AcTPO)12) has been developed as a hemoglobin-based oxygen carrier. While Hb(AcTPO)12 has been shown to exert beneficial effects in a number of models of oxidative injury, its peroxidase activity has not been characterized thus far. In the blood stream, Hb(AcTPO)12 undergoes reduction by ascorbate to its hydroxylamine form Hb(AcTPOH)12. Here we report that Hb(AcTPOH)12exhibits peroxidase activity where H2O2 is utilized for intramolecular oxidation of its TPOH residues to TPO. This represents an unusual redox-catalytic mechanism whereby reduction of H2O2 is achieved at the expense of reducing equivalents of ascorbate converted into those of Hb(AcTPOH)12, a new propensity that cannot be directly associated with ascorbate
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