260 research outputs found

    Comparing Experts and Novices on Scaffolded Data Visualizations using Eye-tracking

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    Spatially-based scientific data visualizations are becoming widely available, yet they are often not optimized for novice audiences. This study follows after an investigation of ex-pert and novice meaning-making from scaffolded data visualizations using clinical inter-views. Using eye-tracking and concurrent interviewing, we examined quantitative fixation and AOI data and qualitative scan path data for two expertise groups (N = 20) on five versions of scaffolded global ocean data visualizations. We found influences of expertise, scaffolding, and trial. In accordance with our clinical interview findings, experts use dif-ferent meaning-making strategies from novices, but novice performance improves with scaffolding and guided practice, providing triangulation. Eye-tracking data also provide insight on meaning-making and effectiveness of scaffolding that clinical interviews alone did not

    Degree correlation effect of bipartite network on personalized recommendation

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    In this paper, by introducing a new user similarity index base on the diffusion process, we propose a modified collaborative filtering (MCF) algorithm, which has remarkably higher accuracy than the standard collaborative filtering. In the proposed algorithm, the degree correlation between users and objects is taken into account and embedded into the similarity index by a tunable parameter. The numerical simulation on a benchmark data set shows that the algorithmic accuracy of the MCF, measured by the average ranking score, is further improved by 18.19% in the optimal case. In addition, two significant criteria of algorithmic performance, diversity and popularity, are also taken into account. Numerical results show that the presented algorithm can provide more diverse and less popular recommendations, for example, when the recommendation list contains 10 objects, the diversity, measured by the hamming distance, is improved by 21.90%.Comment: 9 pages, 3 figure

    catena-Poly[[bis­(pyridine-κN)nickel(II)]-μ-oxalato-κ4 O 1,O 2:O 1′,O 2′]

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    The title compound, [Ni(C2O4)(C5H5N)2]n, was synthesized under hydro­(solvo)thermal conditions. The NiII atom, lying on a twofold rotation axis, has an octa­hedral coordination geometry involving two N atoms from two pyridine ligands and four O atoms from two oxalate ligands. The Ni atoms are connected by the tetra­dentate bridging oxalate ligands into a one-dimensional zigzag chain

    Experimental and theoretical investigations of copper (I/II) complexes with triazine-pyrazole derivatives as ligands and their in situ C-N bond cleavage

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    Two copper complexes, Cu(SCN)(MpzT-(EtO)) (1) (MpzT-(EtO) = L3) and CuCl(HO)(MpzT-O) (2) (MpzT-O = L4) were synthesized by the reaction of 2,4,6-tri(3,5-dimethylpyrazol-1-yl)-1,3,5-triazine (L1) or 2,4,6-tri(1H-pyrazol-1-yl)-1,3,5-triazine (L2) with CuCl·2HO in anhydrous ethanol and methanol, respectively. The complexes were characterized by elemental analysis, IR spectroscopy, thermogravimetric analysis, single crystal X-ray diffraction and X-ray powder diffraction. The structural characterizations and quantum mechanical calculations of the two complexes were analyzed in detail. It was found that an in site reaction occurred during the synthesis process of complexes 1 and 2, likely due to catalytic property of copper ions which leads to the C-N bond cleavage to generate new organic species, namely, MpzT-(EtO) (L3) and MpzT-O (L4)

    CpG-binding protein CFP1 promotes ovarian cancer cell proliferation by regulating BST2 transcription

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    Epigenetic alterations have been functionally linked to ovarian cancer development and occurrence. The CXXC zinc finger protein 1 (CFP1) is an epigenetic regulator involved in DNA methylation and histone modification in mammalian cells. However, its role in ovarian cancer cells is unknown. Here, we show that CFP1 protein is highly expressed in human ovarian cancer tissues. Loss of CFP1 inhibited the growth of human ovarian cancer cells, promoted apoptosis, and increased senescence. CFP1 knockdown resulted in reduced levels of SETD1 (a CFP1 partner) and histone H3 trimethylation at the fourth lysine residue (H3K4me3). RNA-sequencing revealed that deletion of CFP1 resulted in mRNA reduction of bone marrow stromal cell antigen 2 (BST2). Bioinformatics analysis and chromatin immunoprecipitation showed that CFP1 binds to the promoter of BST2 and regulates its transcription directly. Overexpression of BST2 rescued the growth inhibitory effect of CFP1 loss. Furthermore, depletion of cullin-RING ubiquitin ligases 4 (CRL4) components ROC1 or CUL4A had significantly inhibited the expression of CFP1 and BST2 similar to MLN4924 treatment that blocked cullin neddylation and inactivated CRL4s. In conclusion, CFP1 promotes ovarian cancer cell proliferation and apoptosis by regulating the transcription of BST2, and the expression of CFP1 was affected by CRL4 ubiquitin ligase complex

    The lncRNA MALAT1 rs619586 G Variant Confers Decreased Susceptibility to Recurrent Miscarriage

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    Cardiovascula disease and recurrent miscarriage have shared risk factors, and some cardiovascular disease-related candidate genes have been confirmed to be associated with recurrent miscarriage. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA (lncRNA) that is considered to be associated with susceptibility to cardiovascular disease. However, whether lncRNA MALAT1 polymorphisms are related to recurrent miscarriage susceptibility is unclear. We genotyped three lncRNA MALAT1 polymorphisms (rs591291, rs619586, and rs3200401) in 284 patients and 392 controls using TaqMan methods. Logistic regression was used to evaluate the odds ratios (ORs) and 95% confidence intervals (CIs) adjusted for age. Our results showed that the rs619586 G variant had protective effects against recurrent miscarriage (AG vs. AA: adjusted OR = 0.670, 95% CI = 0.457–0.982, p = 0.040; GG vs. AA: adjusted OR = 0.278, 95% CI = 0.079–0.975, p = 0.046; GG/AG vs. AA adjusted OR = 0.621, 95% CI = 0.429–0.900, p = 0.012). In a combined analyses of protective genotypes, with regard to the three single nucleotide polymorphisms (SNPs), we found that individuals with two or three protective genotypes exhibited a significantly lower risk of recurrent miscarriage than those with no or only one protective genotype (adjusted OR = 0.369, 95% CI = 0.199–0.684, p = 0.002). Moreover, the decrease in recurrent miscarriage risk with two or three protective genotypes was most pronounced in women less than 35 years of age (OR = 0.290, 95% CI = 0.142–0.589, p < 0.001) and in women with 2–3 miscarriages (adjusted OR = 0.270, 95% CI = 0.126–0.580, p < 0.001). In conclusion, our study suggests that the rs619586 G variant may have potential protective effects conferring a decreased risk of recurrent miscarriage in the southern Chinese population

    S1PR1 regulates ovarian cancer cell senescence through the PDK1-LATS1/2-YAP pathway

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    Cell senescence deters the activation of various oncogenes. Induction of senescence is, therefore, a potentially effective strategy to interfere with vital processes in tumor cells. Sphingosine-1-phosphate receptor 1 (S1PR1) has been implicated in various cancer types, including ovarian cancer. The mechanism by which S1PR1 regulates ovarian cancer cell senescence is currently elusive. In this study, we demonstrate that S1PR1 was highly expressed in human ovarian cancer tissues and cell lines. S1PR1 deletion inhibited the proliferation and migration of ovarian cancer cells. S1PR1 deletion promoted ovarian cancer cell senescence and sensitized ovarian cancer cells to cisplatin chemotherapy. Exposure of ovarian cancer cells to sphingosine-1-phosphate (S1P) increased the expression of 3-phosphatidylinositol-dependent protein kinase 1 (PDK1), decreased the expression of large tumor suppressor 1/2 (LATS1/2), and induced phosphorylation of Yes-associated protein (p-YAP). Opposite results were obtained in S1PR1 knockout cells following pharmacological inhibition. After silencing LATS1/2 in S1PR1-deficient ovarian cancer cells, senescence was suppressed and S1PR1 expression was increased concomitantly with YAP expression. Transcriptional regulation of S1PR1 by YAP was confirmed by chromatin immunoprecipitation. Accordingly, the S1PR1-PDK1-LATS1/2-YAP pathway regulates ovarian cancer cell senescence and does so through a YAP-mediated feedback loop. S1PR1 constitutes a druggable target for the induction of senescence in ovarian cancer cells. Pharmacological intervention in the S1PR1-PDK1-LATS1/2-YAP signaling axis may augment the efficacy of standard chemotherapy.</p
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