Sentiment Analysis of Tourism Reviews: An exploratory study based on CNNs built on LSTM model

This study is to develop a sentiment analysis system for customers’ review on a scenic site. It is based on Convolutional Neural Networks (CNNs) built on Long Short-Term Memory (LSTM) models for text feature extraction under a deep learning framework. The CNNs built on LSTM models applies convolutional filters of CNNs repeatedly operate on the output matrix of LSTM to obtain robust text feature vector. In this study, the optimal parameter configurations for each component of CNNs and LSTM are given individually in the first place. Then, the entire optimal parameter configuration for the integration recognition frame of the system is identified around the optimum of each component. The results demonstrate that, by employing such a method, the accuracy for sentiment analysis with CNNs built on LSTM model, compared with a single CNNs or LSTM model, is improved by 3.13% and 1.71% respectively

Multi-level reproducibility of signature hubs in human interactome for breast cancer metastasis

<p>Abstract</p> <p>Background</p> <p>It has been suggested that, in the human protein-protein interaction network, changes of co-expression between highly connected proteins ("hub") and their interaction neighbours might have important roles in cancer metastasis and be predictive disease signatures for patient outcome. However, for a cancer, such disease signatures identified from different studies have little overlap.</p> <p>Results</p> <p>Here, we propose a systemic approach to evaluate the reproducibility of disease signatures at multiple levels, on the basis of some statistically testable biological models. Using two datasets for breast cancer metastasis, we showed that different signature hubs identified from different studies were highly consistent in terms of significantly sharing interaction neighbours and displaying consistent co-expression changes with their overlapping neighbours, whereas the shared interaction neighbours were significantly over-represented with known cancer genes and enriched in pathways deregulated in breast cancer pathogenesis. Then, we showed that the signature hubs identified from the two datasets were highly reproducible at the protein interaction and pathway levels in three other independent datasets.</p> <p>Conclusions</p> <p>Our results provide a possible biological model that different signature hubs altered in different patient cohorts could disturb the same pathways associated with cancer metastasis through their interaction neighbours.</p

Role of oxidative stress in trichloroethylene-induced toxicity

Trichloroethylene (TCE) is a common industrial organic solvent and environmental contaminant. People are exposed to TCE through occupational contact or environmental pollution, which leads to serious human health hazards. A large number of studies have shown that oxidative stress plays an important role in the TCE-induced multi-target organ toxicity. However, the research of related signaling pathways remains to be deepened. In this review, we summarized the epidemiological, animal, and cellular studies correlated to liver toxicity, kidney toxicity, cardiac developmental toxicity, placental developmental toxicity, neurodevelopmental toxicity, and autoimmune response induced by TCE. In addition, the possible molecular mechanisms of oxidative stress in TCE-induced toxicity were concluded, including DNA damage, mitochondrial dysfunction, cell apoptosis, and abnormal activation of the immune system. Through literature review, we proposed that nuclear factor E2 related factor 2 may play an important role in mediating TCE-induced target organ toxicity, providing a theoretical basis for the prevention and treatment of adverse health effects caused by TCE

Coordinated control strategy of reactive power compensation based on a flexible distribution network transformer

In order to solve the problem of the power quality caused by distributed power access to the distribution network, this paper proposes a coordinated control strategy of reactive power compensation based on a flexible distribution transformer. First, the working principle of the flexible distribution transformer is analyzed, and the mathematical model of energy acquisition and the regulation converter of the flexible distribution transformer are studied as well. The device-level control strategies of energy acquisition and regulation converters are proposed, respectively. Then, in order to maintain the stability of the bus voltage and quickly respond to the reactive power changes of the system, a coordinated control strategy for the reactive power compensation of flexible distribution transformers is proposed. The priority herein is to maximize the reactive power compensation capacity of the energy harvesting converter. When the energy harvesting converter reaches the compensation upper limit, the control converter is used for reactive power compensation to further suppress the grid voltage fluctuation. Finally, it is verified through simulations that the flexible distribution transformer can realize the reactive power compensation of the distribution network and effectively improve the power quality of the distribution network

FAK Promotes Early Osteoprogenitor Cell Proliferation by Enhancing mTORC1 Signaling

Focal adhesion kinase (FAK) has important functions in bone homeostasis but its role in early osteoprogenitor cells is unknown. We show herein that mice lacking FAK in Dermo1- expressing cells exhibited low bone mass and decreased osteoblast number. Mechanistically, FAK- deficient early osteoprogenitor cells had decreased proliferation and significantly reduced mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling, a central regulator of cell growth and proliferation. Furthermore, our data showed that the pharmacological inhibition of FAK kinase- dependent function alone was sufficient to decrease the proliferation and compromise the mineralization of early osteoprogenitor cells. In contrast to the Fak deletion in early osteoprogenitor cells, FAK loss in Col3.6 Cre- targeted osteoblasts did not cause bone loss, and Fak deletion in osteoblasts did not affect proliferation, differentiation, and mTORC1 signaling but increased the level of active proline- rich tyrosine kinase 2 (PYK2), which belongs to the same non- receptor tyrosine kinase family as FAK. Importantly, mTORC1 signaling in bone marrow stromal cells (BMSCs) was reduced if FAK kinase was inhibited at the early osteogenic differentiation stage. In contrast, mTORC1 signaling in BMSCs was not affected if FAK kinase was inhibited at a later osteogenic differentiation stage, in which, however, the concomitant inhibition of both FAK kinase and PYK2 kinase reduced mTORC1 signaling. In summary, our data suggest that FAK promotes early osteoprogenitor cell proliferation by enhancing mTORC1 signaling via its kinase- dependent function and the loss of FAK in osteoblasts can be compensated by the upregulated active PYK2. © 2020 American Society for Bone and Mineral Research.Schematic model of the differential roles of FAK in the cells of osteoblast lineage. The model depicts the mechanisms of FAK action at three distinct stages of osteoblast lineage in which the roles of FAK have been addressed by genetic and pharmacological approaches as well as the respective Cre transgenes used to target Fak, including Dermo1- Cre (this study), Osterix- Cre,(10) Col3.6- Cre (this study), and Col2.3- Cre.(9) Red - indicates that the loss of FAK in osteoblasts can be compensated by the upregulated active PYK2.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/3/jbmr4029-sup-0001-Supinfo.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/2/jbmr4029_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/1/jbmr4029.pd

Identification of the osteoarthritis signature gene PDK1 by machine learning and its regulatory mechanisms on chondrocyte autophagy and apoptosis

BackgroundOsteoarthritis (OA) is a degenerative joint disease frequently diagnosed in the elderly and middle-aged population. However, its specific pathogenesis has not been clarified. This study aimed to identify biomarkers for OA diagnosis and elucidate their potential mechanisms for restoring OA-dysregulated autophagy and inhibiting chondrocyte apoptosis in vitro.Material and methodsTwo publicly available transcriptomic mRNA OA-related datasets (GSE10575 and GSE51588) were explored for biomarker identification by least absolute shrinkage and selection operator (LASSO) regression, weighted gene co-expression network analysis (WGCNA), and support vector machine recursive feature elimination (SVM-RFE). We applied the GSE32317 and GSE55457 cohorts to validate the markers’ efficacy for diagnosis. The connections of markers to chondrocyte autophagy and apoptosis in OA were also comprehensively explored in vitro using molecular biology approaches, including qRT-PCR and Western blot.ResultsWe identified 286 differentially expressed genes (DEGs). These DEGs were enriched in the ECM-receptor interaction and PI3K/AKT signaling pathway. After external cohort validation and protein-protein interaction (PPI) network construction, PDK1 was finally identified as a diagnostic marker for OA. The pharmacological properties of BX795-downregulated PDK1 expression inhibited LPS-induced chondrocyte inflammation and apoptosis and rescued OA-dysregulated autophagy. Additionally, the phosphorylation of the mediators associated with the MAPK and PI3K/AKT pathways was significantly downregulated, indicating the regulatory function of PDK1 in apoptosis and autophagy via MAPK and PI3K/AKT-associated signaling pathways in chondrocytes. A significantly positive association between the PDK1 expression and Neutrophils, Eosinophils, Plasma cells, and activated CD4 memory T cells, as well as an evident negative correlation between T cells follicular helper and CD4 naive T cells, were detected in the immune cell infiltration analysis.ConclusionsPDK1 can be used as a diagnostic marker for OA. Inhibition of its expression can rescue OA-dysregulated autophagy and inhibit apoptosis by reducing the phosphorylation of PI3K/AKT and MAPK signaling pathways

Observation of intervalley quantum interference in epitaxial monolayer WSe2

Monolayer (ML) transition metal dichalcogenides (TMDs) have been attracting great research attentions lately for their extraordinary properties, in particular the exotic spin-valley coupled electronic structures that promise future spintronic and valleytronic applications1-3. The energy bands of ML TMDs have well separated valleys that constitute effectively an extra internal degree of freedom for low energy carriers3-12. The large spin-orbit coupling in the TMDs makes the spin index locked to the valley index, which has some interesting consequences such as the magnetoelectric effects in 2H bilayers13. A direct experimental characterization of the spin-valley coupled electronic structure can be of great interests for both fundamental physics and device applications. In this work, we report the first experimental observation of the quasi-particle interference (QPI) patterns in ML WSe2 using low-temperature (LT) scanning tunneling microscopy/spectroscopy (STM/S). We observe intervalley quantum interference involving the Q-valleys in the conduction band due to spin-conserved scattering processes, while spin-flip intervalley scattering is absent. This experiment establishes unequivocally the presence of spin-valley coupling and affirms the large spin-splitting at the Q valleys. Importantly, the inefficient spin-flip intervalley scattering implies long valley and spin lifetime in ML WSe2, which represents a key figure of merit for valley-spintronic applications.Comment: 15 pages, 4 figure

Dense network of one-dimensional mid-gap metallic modes in monolayer MoSe2 and their spatial undulations

We report the observation of a dense triangular network of one-dimensional (1D) metallic modes in a continuous and uniform monolayer of MoSe2 grown by molecular-beam epitaxy. High-resolution transmission electron microscopy and scanning tunneling microscopy and spectroscopy (STM/STS) studies show these 1D modes are mid-gap states at inversion domain boundaries. STM/STS measurements further reveal intensity undulations of the metallic modes, presumably arising from the superlattice potentials due to moire pattern and the quantum confinement effect. A dense network of the metallic modes with high density of states is of great potential for heterocatalysis applications. The interconnection of such mid-gap 1D conducting channels may also imply new transport behaviors distinct from the 2D bulk

Three Gorges Dam: Friend or Foe of Riverine Greenhouse Gases?

International audienceDams are often regarded as greenhouse gas (GHG) emitters. However, our study indicated that the world's largest dam, the Three Gorges Dam (TGD), has caused significant drops in annual average emissions of CO$_2$, CH$_4$ and N$_2$O over 4300 km along the Yangtze River, accompanied by remarkable reductions in the annual export of CO$_2$ (79%), CH$_4$ (50%) and N$_2$O (9%) to the sea. Since the commencement of its operation in 2003, the TGD has altered the carbonate equilibrium in the reservoir area, enhanced methanogenesis in the upstream, and restrained methanogenesis and denitrification via modifying anoxic habitats through long-distance scouring in the downstream. These findings suggest that 'large-dam effects' are far beyond our previous understanding spatiotemporally, which highlights the fundamental importance of whole-system budgeting of GHGs under the profound impacts of huge dams