1,342 research outputs found

    Social Capital and Technological Literacy in Taiwan

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    The burgeoning interest in social capital within the technology community represents a welcome move towards a concern for the social elements of technological adaptation and capacity. Since technology plays an ever larger role in our daily life, it is necessary to articulate social capital and its relationship to technological literacy. A nationwide data was collected by area sampling, and position generator was used to measure social capital. Regression model was constructed for technological literacy. Age, gender, education, income, web access, and social capital were included as independent variables. The results show that age, gender, education, web access, and social capital were good predictors of technological literacy. It is concluded that social capital is helpful in coping with rapid technological change. Theoretical and empirical implications and future research are discussed

    Prevalence and Associated Metabolic Factors of Gallstone Disease in the Elderly Agricultural and Fishing Population of Taiwan

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    Purpose. To evaluate sex-related differences in the prevalence of and cardiovascular risk factors related to gallstone disease (GSD) in an elderly agricultural and fishing population of Taipei, Taiwan. Methods. The study sample consisted of 6511 healthy elderly participants (3971 men and 2540 women) who were voluntarily admitted to a teaching hospital for a physical checkup in 2010. The participants’ blood samples and real-time ultrasound fatty liver results were collected. Results. The prevalence of GSD in the study population was 13.2%, which increased significantly with population age (P<.0001). Women were associated with significantly higher GSD prevalence than men (14.8% versus 12.2%; for the chi-square test, P=.003). In a multiple logistic regression analysis, female sex, older age, and metabolic syndrome (MetS) were significantly associated with GSD. Multiple logistic regression analysis also revealed that obesity (odds ratio OR=1.26, 95% confidence interval (CI): 1.09–1.44) and metabolic factors (one or 2 versus none, OR=1.48, 95% CI: 1.08–1.76) were significantly associated with GSD in women but not in men. Conclusion. In the study population, female sex, older age, and MetS were associated with higher GSD prevalence. The population exhibited other sex-related differences

    Coregulation of transcription factors and microRNAs in human transcriptional regulatory network

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    <p>Abstract</p> <p>Background</p> <p>MicroRNAs (miRNAs) are small RNA molecules that regulate gene expression at the post-transcriptional level. Recent studies have suggested that miRNAs and transcription factors are primary metazoan gene regulators; however, the crosstalk between them still remains unclear.</p> <p>Methods</p> <p>We proposed a novel model utilizing functional annotation information to identify significant coregulation between transcriptional and post-transcriptional layers. Based on this model, function-enriched coregulation relationships were discovered and combined into different kinds of functional coregulation networks.</p> <p>Results</p> <p>We found that miRNAs may engage in a wider diversity of biological processes by coordinating with transcription factors, and this kind of cross-layer coregulation may have higher specificity than intra-layer coregulation. In addition, the coregulation networks reveal several types of network motifs, including feed-forward loops and massive upstream crosstalk. Finally, the expression patterns of these coregulation pairs in normal and tumour tissues were analyzed. Different coregulation types show unique expression correlation trends. More importantly, the disruption of coregulation may be associated with cancers.</p> <p>Conclusion</p> <p>Our findings elucidate the combinatorial and cooperative properties of transcription factors and miRNAs regulation, and we proposes that the coordinated regulation may play an important role in many biological processes.</p

    Crosstalk between transcription factors and microRNAs in human protein interaction network

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    <p>Abstract</p> <p>Background</p> <p>Gene regulatory networks control the global gene expression and the dynamics of protein output in living cells. In multicellular organisms, transcription factors and microRNAs are the major families of gene regulators. Recent studies have suggested that these two kinds of regulators share similar regulatory logics and participate in cooperative activities in the gene regulatory network; however, their combinational regulatory effects and preferences on the protein interaction network remain unclear.</p> <p>Methods</p> <p>In this study, we constructed a global human gene regulatory network comprising both transcriptional and post-transcriptional regulatory relationships, and integrated the protein interactome into this network. We then screened the integrated network for four types of regulatory motifs: single-regulation, co-regulation, crosstalk, and independent, and investigated their topological properties in the protein interaction network.</p> <p>Results</p> <p>Among the four types of network motifs, the crosstalk was found to have the most enriched protein-protein interactions in their downstream regulatory targets. The topological properties of these motifs also revealed that they target crucial proteins in the protein interaction network and may serve important roles of biological functions.</p> <p>Conclusions</p> <p>Altogether, these results reveal the combinatorial regulatory patterns of transcription factors and microRNAs on the protein interactome, and provide further evidence to suggest the connection between gene regulatory network and protein interaction network.</p

    Poly[(acetato-κ2 O,O′)aqua­(μ4-1H-benzimidazole-5,6-dicarboxyl­ato-κ5 N 3:O 5,O 5′:O 5,O 6:O 6′)praseodymium(III)]

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    In the title complex, [Pr(C9H4N2O4)(C2H3O2)(H2O)]n, the PrIII ion is coordinated by five O atoms and one N atom from four benzimidazole-5,6-dicarboxyl­ate ligands, two O atoms from an acetate ligand and one water mol­ecule, giving a tricapped trigonal-prismatic geometry. The benzimidazole-5,6-dicarboxyl­ate and acetate ligands connect the PrIII ions, forming a layer in the ac plane; the layers are further linked by N—H⋯O and O—H⋯O hydrogen bonding and π–π stacking inter­actions between neighboring pyridine rings [the centroid–centroid distance is 3.467 (1) Å], assembling a three-dimensional supra­molecular network. The acetate methyl group is disordered over two positions with site-occupancy factors of 0.75 and 0.25

    6-Mercaptopurine attenuates tumor necrosis factor-α production in microglia through Nur77-mediated transrepression and PI3K/Akt/mTOR signaling-mediated translational regulation

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    Physical interaction between Nur77 and p65. BV-2 cells were pretreated with 6-MP (50 μM) for 16 h followed by exposure to LPS (100 ng/ml) for 60 min. Nuclear extracts were harvested for immunoprecipitation (IP) experiments using anti-Nur77 and anti-p65 antibodies. Immunoblot (IB) analyses of the immunoprecipitates were performed using these antibodies. The immunoblots are representative of three independent experiments. (TIF 280 kb

    The Induction of Apoptosis by SV40 T Antigen Correlates with c-junOverexpression

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    AbstractSimian virus (SV40) T antigen shares many characteristics with adenovirus E1A which is known to induce apoptosis. To verify the potential of SV40 T antigen-mediated apoptosis, we stably expressed T antigen in immortalized human epithelial cells (Z172 and HaCaT). We found that SV40 T antigen could directly cause apoptosis in 22–27% of these cells under normal growth condition as measured by chromatin condensation and nucleosomal fragmentation. The apoptosis of HaCaT cells which contain mutant p53 suggests the p53-independent nature of T antigen-mediated apoptosis. T antigen-induced apoptosis was associated with increased expression of c-Jun protein. Moreover, the overexpression of c-junalone in these cells also induced apoptosis, indicating that c-junmight play an important role in T antigen-induced apoptosis
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