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Stock movement prediction is one of the most challenging problems in time series analysis due to the stochastic nature of financial markets. In recent years, a plethora of statistical methods and machine learning algorithms were proposed for stock movement prediction. Specifically, deep learning models are increasingly applied for the prediction of stock movement. The success of deep learning models relies on the assumption that massive training data are available. However, this assumption is impractical for stock movement prediction. In stock markets, a large number of stocks do not have enough historical data, especially for the companies which underwent initial public offering in recent years. In these situations, the accuracy of deep learning models to predict the stock movement could be affected. To address this problem, in this paper, we propose novel instance-based deep transfer learning models with attention mechanism. In the experiments, we compare our proposed methods with state-of-the-art prediction models. Experimental results on three public datasets reveal that our proposed methods significantly improve the performance of deep learning models when limited training data are available.
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The key challenge of Unsupervised Domain Adaptation (UDA) for analyzing time series data is to learn domain-invariant representations by capturing complex temporal dependencies. In addition, existing unsupervised domain adaptation methods for time series data are designed to align marginal distribution between source and target domains. However, existing UDA methods (e.g. R-DANN Purushotham et al. (2017), VRADA Purushotham et al. (2017), CoDATS Wilson et al. (2020)) neglect the conditional distribution discrepancy between two domains, leading to misclassification of the target domain. Therefore, to learn domain-invariant representations by capturing the temporal dependencies and to reduce the conditional distribution discrepancy between two domains, a novel Attentive Recurrent Adversarial Domain Adaptation with Top-k time series pseudo-labeling method called ARADA-TK is proposed in this paper. In the experiments, our proposed method was compared with the state-of-the-art UDA methods (R-DANN, VRADA and CoDATS). Experimental results on four benchmark datasets revealed that ARADA-TK achieves superior classification accuracy when it is compared to the competing methods.
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Approximately 50 million people are suffering from epilepsy worldwide. Corals have been used for treating epilepsy in traditional Chinese medicine, but the mechanism of this treatment is unknown. In this study, we analyzed the transcriptome of the branching coral Acropora digitifera and obtained its Kyoto Encyclopedia of Genes and Genomes (KEGG), EuKaryotic Orthologous Groups (KOG) and Gene Ontology (GO) annotation. Combined with multiple sequence alignment and phylogenetic analysis, we discovered three polypeptides, we named them AdKuz1, AdKuz2 and AdKuz3, from A. digitifera that showed a close relationship to Kunitz-type peptides. Molecular docking and molecular dynamics simulation indicated that AdKuz1 to 3 could interact with GABAA receptor but AdKuz2–GABAA remained more stable than others. The biological experiments showed that AdKuz1 and AdKuz2 exhibited an anti-inflammatory effect by decreasing the aberrant level of nitric oxide (NO), IL-6, TNF-α and IL-1β induced by LPS in BV-2 cells. In addition, the pentylenetetrazol (PTZ)-induced epileptic effect on zebrafish was remarkably suppressed by AdKuz1 and AdKuz2. AdKuz2 particularly showed superior anti-epileptic effects compared to the other two peptides. Furthermore, AdKuz2 significantly decreased the expression of c-fos and npas4a, which were up-regulated by PTZ treatment. In addition, AdKuz2 reduced the synthesis of glutamate and enhanced the biosynthesis of gamma-aminobutyric acid (GABA). In conclusion, the results indicated that AdKuz2 may affect the synthesis of glutamate and GABA and enhance the activity of the GABAA receptor to inhibit the symptoms of epilepsy. We believe, AdKuz2 could be a promising anti-epileptic agent and its mechanism of action should be further investigated.
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Neuropeptides are a group of neuronal signaling molecules that regulate physiological and behavioral processes in animals. Here, we used in silico mining to predict the polypeptide composition of available transcriptomic data of Turbinaria peltata. In total, 118 transcripts encoding putative peptide precursors were discovered. One neuropeptide Y/F-like peptide, named TpNPY, was identified and selected for in silico structural, in silico binding, and pharmacological studies. In our study, the anti-inflammation effect of TpNPY was evaluated using an LPS-stimulated C8-D1A astrocyte cell model. Our results demonstrated that TpNPY, at 0.75–3 μM, inhibited LPS-induced NO production and reduced the expression of iNOS in a dose-dependent manner. Furthermore, TpNPY reduced the secretion of proinflammatory cytokines. Additionally, treatment with TpNPY reduced LPS-mediated elevation of ROS production and the intracellular calcium concentration. Further investigation revealed that TpNPY downregulated the IKK/IκB/NF-κB signaling pathway and inhibited expression of the NLRP3 inflammasome. Through molecular docking and using an NPY receptor antagonist, TpNPY was shown to have the ability to interact with the NPY Y1 receptor. On the basis of these findings, we concluded that TpNPY might prevent LPS-induced injury in astrocytes through activation of the NPY-Y1R.