948 research outputs found

    Adversarial Prediction Framework for Information Retrieval and Natural Language Processing Metrics

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    Many Information Retrieval (IR) and Natural Language Processing (NLP) tasks require predicting structured objects (e.g., sequences, rankings, matchings, parse trees) that are evaluated using F-score (i.e., the harmonic mean of precision and recall), precision at k (P@k, which limits the number of positive predictions to k), discounted cumulative gain (DCG), alignment error rate (AER), Hamming loss (i.e., accuracy) or other multivariate performance measures. Due to the non-convexity of most of the multivariate performance metrics, and the computational intractability of optimizing empirical risk over those metrics, traditional Machine Learning algorithms use convex surrogates (e.g., log-loss for Logistic Regression, hinge-loss for Support Vector Machine) as the approximations for empirical risk optimization. However, these approximations introduce a mismatch between the learner's objective and the desired application performance. How can Machine Learning algorithms' predictions be more closely aligned with application performance measures in Information Retrieval and Natural Language Processing? In this thesis, we focus on answering this question by building an adversarial prediction framework - Multivariate Prediction Game (MPG) - for the metrics that are widely used in Information Retrieval and Natural Language Processing areas. MPG treats the multivariate prediction as an adversarial zero-sum game between a loss-minimizing prediction player and a loss-maximizing evaluation player constrained to match specified properties of training data. By solving the problem of effectively finding the best responses to the opponent's strategies, and applying the double oracle constraint generation method, the framework avoids the non-convexity of empirical risk minimization, and hence directly optimizes the metrics. In this thesis, we first introduce the background of our research with its related works. Then, the Multivariate Prediction Game framework is explained in detail. For each metric of predicting structure, we give the corresponding algorithm for effectively finding the best responses. Finally, the MPGs are evaluated on several widely used data sets in Information Retrieval and Natural Language Processing areas to demonstrate their effectiveness

    sj-pdf-1-imr-10.1177_03000605231194514 - Supplemental material for Retinal artery occlusion after facial filler injection in a patient with patent foramen ovale: a case report and literature review

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    Supplemental material, sj-pdf-1-imr-10.1177_03000605231194514 for Retinal artery occlusion after facial filler injection in a patient with patent foramen ovale: a case report and literature review by Mingwei Si and Hong Wang in Journal of International Medical Research</p

    sj-pdf-2-imr-10.1177_03000605231194514 - Supplemental material for Retinal artery occlusion after facial filler injection in a patient with patent foramen ovale: a case report and literature review

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    Supplemental material, sj-pdf-2-imr-10.1177_03000605231194514 for Retinal artery occlusion after facial filler injection in a patient with patent foramen ovale: a case report and literature review by Mingwei Si and Hong Wang in Journal of International Medical Research</p

    Prenatal Nicotine and Maternal Deprivation Stress De-Regulate the Development of CA1, CA3, and Dentate Gyrus Neurons in Hippocampus of Infant Rats

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    <div><p>Adverse experiences by the developing fetus and in early childhood are associated with profound effects on learning, emotional behavior, and cognition as a whole. In this study we investigated the effects of prenatal nicotine exposure (NIC), postnatal maternal deprivation (MD) or the combination of the two (NIC+MD) to determine if hippocampal neuron development is modulated by exposure to drugs of abuse and/or stress. Growth of rat offspring exposed to MD alone or NIC+MD was repressed until after weaning. In CA1 but not CA3 of postnatal day 14 (P14) pups, MD increased pyramidal neurons, however, in dentate gyrus (DG), decreased granule neurons. NIC had no effect on neuron number in CA1, CA3 or DG. Unexpectedly, NIC plus MD combined caused a synergistic increase in the number of CA1 or CA3 neurons. Neuron density in CA regions was unaffected by treatment, but in the DG, granule neurons had a looser packing density after NIC, MD or NIC+MD exposure. When septotemporal axes were analyzed, the synergism of stress and drug exposure in CA1 and CA3 was associated with rostral, whereas MD effects were predominantly associated with caudal neurons. TUNEL labeling suggests no active apoptosis at P14, and doublecortin positive neurons and mossy fibers were diminished in NIC+MD relative to controls. The laterality of the effect of nicotine and/or maternal deprivation in right versus left hippocampus was also analyzed and found to be insiginificant. We report for the first time that early life stressors such as postnatal MD and prenatal NIC exposure, when combined, may exhibit synergistic consequences for CA1 and CA3 pyramidal neuron development, and a potential antagonistic influence on developing DG neurons. These results suggest that early stressors may modulate neurogenesis, apoptosis, or maturation of glutamatergic neurons in the hippocampus in a region-specific manner during critical periods of neurodevelopment.</p></div

    The expression of miR-122 and IGF1R is negatively correlated in clinical BC tissues.

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    <p>There may be an inverse relationship between the expression of miR-122 and IGF1R.</p

    IGF1R is directly targeted by miR-122.

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    <p>(A) IGF1R 3′UTR and IGF1R 3′UTR-MT were inserted into the region immediately downstream of the luciferase gene in pGL3 vector. (B) Dual luciferase reporter assays were performed. The expression of the reporter containing IGF1R 3′UTR was suppressed by miR-122, but not in the mutated construct. qRT–PCR (C) and Western blot (D) analyses were performed to examine the effects of miR-122 on IGF1R expression in MCF-7 cells. Both precursor and mature IGF1R (2 bands) were suppressed after miR-122 overexpression. The suppression was abolished by transfection of the cells with IGF1R cDNA without 3′UTR. All experiments were carried 3 times independently. *P<0.05 compared to EV group. **P<0.01 compared to EV group.</p

    IGF1R is involved in miR-122-induced growth inhibition in BC cells.

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    <p>(A) MCF-7 cells were infected with Lv-shIGF1R or Lv-miR122. Cell growth rate and cell-cycle distribution were measured. (B) MCF-7 cells were infected with LV-miR122 for 72 hours, followed by infection with LV-IGF1R, and cell proliferation and cell-cycle analysis were then performed. *P<0.05 compared to EV group or comparison between 2 groups as indicated, **P<0.01 compared to EV group or comparison between 2 groups as indicated.</p

    Overexpression of miR-122 suppresses cell proliferation of MCF-7 cells in vitro and in vivo.

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    <p>(A) miR-122 was over-expressed in MCF-7 cells and confirmed by qRT-PCR. (B) Growth curves of miR-122 and EV-infected MCF-7 cells were conducted. (C) Colony formation was assayed in miR-122 and EV-infected cells, and colonies consisting more than 50 cells were counted. (D) Cell cycle progression was assayed using flow cytometric analysis. (E) Tumor size observation in nude mice after the inoculation. The average size of the tumors was measured every 5 days and shown in the curves. (F) Tumor sizes of 3 representative nude mice. The tumor weight was measured. All experiments were carried 3 times independently. *P<0.05 compared to EV group. **P<0.01 compared to EV group.</p

    The expression of miR-122 is suppressed in BC cell lines.

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    <p>The miR-122 expression levels of MCF-7, T47d, MDA-MB-231, BT549 and HBL-100 cells were detected by qRT-PCR. The relative expression of miR-122 was normalized to the endogenous control U6. Each sample was analyzed in triplicate. (*p<0.05, **p<0.01).</p

    Estimated pyramidal or granule cell numbers, volume and density for CA1, CA3 and DG of Sprague Dawley rat hippocampi at P14 (bilateral) after maternal deprivation and/or prenatal nicotine exposure.

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    *<p>Values represent mean ± standard error of the mean (sem); (*) indicates significance compared to control, (#) compared to MD, (+) compared to NIC; */<i>#/+, p≤0.05;</i></p>**<p><i>/##/++, p≤0.01;</i></p>***<p><i>/###/+++, p≤0.001.</i></p
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