Polyline simplification using a region proposal network integrating raster and vector features

ABSTRACTPolyline simplification is crucial for cartography and spatial database management. In recent decades, various rule-based algorithms for vector polyline simplification have been proposed. However, most existing algorithms lack parameter self-adaptive capabilities and require repeated manual parameter adjustments when applied to different polylines. While deep-learning-based methods have recently been introduced for raster polyline image simplification, they cannot achieve end-to-end simplification when the input data and output results are vector polylines. This paper proposes a new deep-learning-based method for vector polyline simplification by integrating both the vector and raster features of the polyline. Specifically, a deep separable convolutional residual neural network was first used to extract the convolutional features of each image. Then, the region proposal network was modified to generate proposal boxes using vector coordinates, and these proposal boxes were used to locate the convolutional feature maps of bends. Finally, convolutional feature maps were fed into a binary classification network to identify unimportant vertices that should be omitted for vector polyline simplification. The experimental results indicated that the proposed method can exploit raster and vector features to achieve automatic and effective polyline simplification without prior map generalization knowledge and manual settings of rules and parameters. The polyline simplification results of the proposed method have a higher compression ratio of coordinate points and lower shape deformation and deviation than the results generated by the classic Wang and Müller (WM) algorithm and Support Vector Machine (SVM) based algorithm, which shows the potential of the proposed method for future applications in map generalization

Does Identification Influence Continuous E-Commerce Consumption? The Mediating Role of Intrinsic Motivations

The motivation behind online consumption behavior is different from that of online social behavior, and research is lacking regarding the impact of identification on e-commerce consumption. The current research examines the influence of identification, which is perceived anonymity, and intrinsic motivation on the continuous purchasing behaviors on retailing e-commerce websites based on self-determination theory. The mediating role of intrinsic motivation was also empirically tested from a sample of 661 frequent consumers using the partial least squares approach. The findings were: (1) Identification negatively influences perceived anonymity, and its low, but significantly positive, influence on continuous e-commerce consumption were totally mediated by perceived competence, perceived autonomy, and perceived relatedness. (2) Perceived anonymity positively influences self-determination factors, which has partly mediating impact between perceived anonymity and continuous consumption. (3) The authenticity and concealment of identity are based on different mechanisms, but both of them are conducive to promoting continuous purchases. On retailing e-commerce websites, customers’ identity management should consider both identification in the background and anonymity perception in the service, and the contributions of the service to promote consumers’ perceived competence and perceived autonomy are important in continuous consumption

EBV-EBNA1 constructs an immunosuppressive microenvironment for nasopharyngeal carcinoma by promoting the chemoattraction of Treg cells

Background Nasopharyngeal carcinoma (NPC) is primarily caused by the Epstein-Barr virus (EBV) infection in NPC endemic areas. EBNA1 is an EBV-encoded nuclear antigen, which plays a critical role in the maintenance and replication of EBV genome. However, the mechanisms of EBNA1-promoted NPC immune escape are unknown. Regulatory T (Treg) cells are among the key regulators in restraining antitumor responses. However, the mechanisms of accumulation of Treg cells in NPC have not been defined. This study attempted to identify the detailed mechanisms of EBNA1 functions as a tumor accelerator to promote NPC immune escape by enhancing chemoattraction of Treg cells.Methods mRNA profiles were determined by next-generation sequencing in NPC cells. In vitro and in vivo assays were performed to analyze the role of EBNA1 in regulation of recruitment of Treg cells. Colocation and coimmunoprecipitation analyzes were used to identify the SMAD3/c-JUN complex. Chromatin immunoprecipitation assay and dual luciferase reporter assays were designed to demonstrate c-JUN binding to miR-200a promoter and miR-200a targeting to CXCL12 3’Untranslated Regions. The hepatocellular carcinoma models were designed to demonstrate universality of the CXCL12-CXCR4-Treg axis in promoting immune evasion of various tumors.Result A novel molecular mechanism was identified that involves EBV-EBNA1-stimulated chemotactic migration of Treg cells toward NPC microenvironment by upregulation of the transforming growth factor-β1 (TGFβ1)-SMAD3-PI3K-AKT-c-JUN-CXCL12-CXCR4 axis and downregulation of miR-200a. EBV-EBNA1 promotes the chemoattraction of Treg cells by governing the protein–protein interactions of the SMAD3/c-JUN complex in a TGFβ1-dependent manner in vitro and in vivo. TGFβ1 suppresses miR-200a by enhancing the SMAD3/c-JUN complex. miR-200a negatively regulates the CXCL12 chemokine by direct targeting of the CXCL12 3’UTR region. However, CXCL12 acts as the target gene of miR-200a and as an inhibitor of miR-200a transcription, and inhibition of miR-200a by CXCL12 is mediated by c-JUN, which directly binds to the miR-200a promoter and forms a c-JUN-miR-200a-CXCL12-c-JUN feedback loop. In addition, enhanced CXCL12 efficiently attracts CXCR4-positive Treg cells to remodel an immunosuppressive microenvironment.Conclusions EBV-EBNA1 promotes chemotactic migration of Treg cells via the TGFβ1-SMAD3-PI3K-AKT-c-JUN-miR-200a-CXCL12-CXCR4 axis in the NPC microenvironment. These results suggest that EBV-EBNA1 may serve as a potential therapeutic target to reshape the NPC microenvironment

Functional Expression, Purification and Identification of Interaction Partners of PACRG

PACRG (Parkin co-regulated gene) shares a bi-directional promoter with the Parkinson’s disease-associated gene Parkin, but the physiological roles of PACRG have not yet been fully elucidated. Recombinant expression methods are indispensable for protein structural and functional studies. In this study, the coding region of PACRG was cloned to a conventional vector pQE80L, as well as two cold-shock vectors pCold II and pCold-GST, respectively. The constructs were transformed into Escherichia coli (DE3), and the target proteins were overexpressed. The results showed that the cold-shock vectors are more suitable for PACRG expression. The soluble recombinant proteins were purified with Ni2+ chelating column, glutathione S-transferase (GST) affinity chromatography and gel filtration. His6 pull down assay and LC-MS/MS were carried out for identification of PACRG-binding proteins in HEK293T cell lysates, and a total number of 74 proteins were identified as potential interaction partners of PACRG. GO (Gene ontology) enrichment analysis (FunRich) of the 74 proteins revealed multiple molecular functions and biological processes. The highest proportion of the 74 proteins functioned as transcription regulator and transcription factor activity, suggesting that PACRG may play important roles in regulation of gene transcription

Exogenous Hydrogen Sulfide Attenuates High Glucose-Induced Cardiotoxicity by Inhibiting NLRP3 Inflammasome Activation by Suppressing TLR4/NF-κB Pathway in H9c2 Cells

Background/Aims: This study aimed to investigate whether exogenous hydrogen sulfide (H2S) confered cardiac protection against high glucose (HG)-induced injury by inhibiting NLRP3 inflammasome activation via a specific TLR4/NF-κB pathway. Methods: H9c2 cardiac cells were exposed to 33 mM glucose for 24 h to induce HG-induced cytotoxicity. The cells were pretreated with NaHS (a donor of H2S) before exposure to HG. Cell viability, cell apoptosis, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and TLR4, NF-κB, NLRP3 inflammasome, IL-1β, IL-18 and caspase-3 expression were measured by standard methods. Results: H2S attenuated HG-induced cell apoptosis, ROS expression and loss of MMP and reduced the expression of NLRP3, ASC, pro-caspase-1, caspase-1, IL-1β, IL-18 and caspase-3. In addition, H2S inhibited the HG-induced activation of TLR4 and NF-κB. Furthermore, NLRP3 inflammasome activation was regulated by the TLR4 and NF-κB pathway. Conclusion: The present study demonstrated for the first time that H2S appears to suppress HG-induced cardiomyocyte inflammation and apoptosis by inhibiting the TLR4/NF-κB pathway and its downstream NLRP3 inflammasome activation. Thus H2S might possess potential in the treatment of diabetic cardiomyopathy

Evaluating the relationship between pain empathy, knowledge and attitudes among nurses in North China: a cross-sectional study

Abstract Background Effective pain management is closely related to nurses’ knowledge, attitudes and empathy regarding pain. Nursing educators and managers should understand the relationship between nurses’ pain management knowledge, attitudes and empathy level, and take targeted measures accordingly. Currently, there is limited study exploring the relationship between pain empathy and pain knowledge and attitudes among nurses in North China. Objectives The purpose of this study was to investigate the level of nurses’ pain management knowledge and attitudes and pain empathy, to analyze the factors influencing pain empathy, and to explore the relationship between these two variables. Design This study was a quantitative, descriptive-correlation design. Setting and participants The study population was registered nurses in North China, the sample included 177 registered nurses in North China. Methods Data were collected with the “General data questionnaire”, “Knowledge and attitudes survey regarding pain” (KASRP) and the “Empathy for pain scale” (EPS) via Wechat mini program “Questionnaire Star”. Results The 177 registered nurses completed the survey. The averege correct rate for KASRP was (51.94 ± 9.44)%, and none of the respondents achieved a percentage score of >80%. The mean score for pain empathy was (2.78 ± 0.78), the empathy reactions dimension was (2.99 ± 0.77), and the body and mind discomfort dimension was (2.71 ± 0.80). The results of multiple stepwise linear regression showed that whether they had received empathy training, whether they had greater trauma or severe pain and whether they had negative emotions were independent influencing factors for EPS scores. Pearson correlation analysis showed that KASRP scores were positively correlated with EPS scores (r = 0.242, P < 0.05). Conclusions The pain knowledge and attitudes of nurses in North China are far from optimal. Nurses have a relatively low accuracy rate in areas such as medication knowledge, assessment of patient pain based on case studies, and handling PRN prescriptions. Nursing educators and administrators need to design some pain management courses in a targeted manner. Nurses’ empathy for pain was at a moderate level. Pain empathy was positively correlated with pain knowledge and attitudes, suggesting that empathy for pain can be developed postnatally

Berberine Protects Human Retinal Pigment Epithelial Cells from Hydrogen Peroxide-Induced Oxidative Damage through Activation of AMPK

Age-related macular degeneration (AMD) is the leading cause of central vision loss in the elderly with less effective treatment, especially for dry AMD (90% of AMD). Although the etiology of this disease is not well elucidated, increasing evidences indicate that excessive reactive oxygen species (ROS) impairing the physiological functions of retinal pigment epithelium (RPE) cells may be one of the main causes. Therefore, it could be a great strategy to find some drugs that can effectively protect RPE cells from oxidative damage which is desired to treat and slow the process of AMD. In the present study, a well-known traditional Chinese medicine berberine (BBR) was found to suppress hydrogen peroxide (H2O2)-induced oxidative damage in D407 cells, a human RPE cell line. Pre-treatment of D407 cells with BBR significantly suppressed H2O2-induced cell apoptosis by restoring abnormal changes in nuclear morphology, preventing the decline of mitochondrial membrane potential, reducing lactate dehydrogenase release and inhibiting caspase 3/7 activities induced by H2O2. Western blot analysis showed that BBR was able to stimulate the phosphorylation/activation of AMPK in a time- and dose-dependent manner in D407 cells, while treatment of cells with AMPK pathway inhibitor Compound C, or knockdown of the AMPK by specific siRNA blocked the effect of BBR. Similar results were obtained in primary cultured human RPE cells. Taken together, these results demonstrated that BBR was able to protect RPE cells against oxidative stress via the activation of AMPK pathway. Our findings also indicate the potential application of BBR in AMD treatment

Leptin-deficient ob/ob mice exhibit periodontitis phenotype and altered oral microbiome

Background and Objective: Leptin-deficient obesity is associated with various systemic diseases including diabetes and low bone mass phenotype. However, the periodontal status of leptin-deficient obese individuals is still unclear. In this study, we aimed to analyze the periodontal status, alveolar bone phenotype, and oral microbiome status in leptin-deficient obese mice (ob/ob mice). Methods: This study used 12-week-old wild-type and ob/ob male mice. The alveolar bone phenotype and periodontal status in the maxilla were analyzed by micro-CT and histological analysis. Osteoclasts in alveolar bone were visualized by TRAP staining. Expressions of inflammatory markers (MMP-9, IL-1β, and TGF-β1) and osteoclastogenic markers (RANKL and OPG) in periodontium were analyzed by immunohistochemistry and RT-qPCR. The oral microbiome was analyzed by 16 S rDNA sequencing. Results: CEJ-ABC distance in maxillary molars (M1-M3) of ob/ob mice was significantly higher compared with that of wild-type. The alveolar bone BV/TV ratio was reduced in ob/ob mice compared with wild-type. Higher numbers of osteoclasts were observed in ob/ob mice alveolar bone adjacent to the molar root. Epithelial hyperplasia in gingiva and disordered periodontal ligaments was observed in ob/ob mice. RANKL/OPG expression ratio was increased in ob/ob mice compared with wild-type. Expressions of inflammatory markers MMP-9, IL-1β, and TGF-β1 were increased in ob/ob mice compared with wild-type. Oral microbiome analysis showed that beneficial bacteria Akkermansia and Ruminococcaceae_UCG_014 were more abundant in the wild-type mice while the inflammation-related Flavobacterium was more abundant in ob/ob mice. Conclusion: In conclusion, ob/ob mice showed higher expressions of inflammatory factors, increased alveolar bone loss, lower abundance of the beneficial bacteria, and higher abundance of inflammatory bacteria in the oral cavity, suggesting leptin-deficient obesity as a risk factor for periodontitis development in ob/ob mice