513 research outputs found

    Reuse of imputed data in microarray analysis increases imputation efficiency

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    BACKGROUND: The imputation of missing values is necessary for the efficient use of DNA microarray data, because many clustering algorithms and some statistical analysis require a complete data set. A few imputation methods for DNA microarray data have been introduced, but the efficiency of the methods was low and the validity of imputed values in these methods had not been fully checked. RESULTS: We developed a new cluster-based imputation method called sequential K-nearest neighbor (SKNN) method. This imputes the missing values sequentially from the gene having least missing values, and uses the imputed values for the later imputation. Although it uses the imputed values, the efficiency of this new method is greatly improved in its accuracy and computational complexity over the conventional KNN-based method and other methods based on maximum likelihood estimation. The performance of SKNN was in particular higher than other imputation methods for the data with high missing rates and large number of experiments. Application of Expectation Maximization (EM) to the SKNN method improved the accuracy, but increased computational time proportional to the number of iterations. The Multiple Imputation (MI) method, which is well known but not applied previously to microarray data, showed a similarly high accuracy as the SKNN method, with slightly higher dependency on the types of data sets. CONCLUSIONS: Sequential reuse of imputed data in KNN-based imputation greatly increases the efficiency of imputation. The SKNN method should be practically useful to save the data of some microarray experiments which have high amounts of missing entries. The SKNN method generates reliable imputed values which can be used for further cluster-based analysis of microarray data

    Cases of ethical violation in research publications: through editorial decision making process

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    Purpose – To improve and strengthen existing publication and research ethics, KODISA has identified and presented various cases which have violated publication and research ethics and principles in recent years. The editorial office of KODISA has been providing and continues to provide advice and feedback on publication ethics to researchers during peer review and editorial decision making process. Providing advice and feedback on publication ethics will ensure researchers to have an opportunity to correct their mistakes or make appropriate decisions and avoid any violations in research ethics. The purpose of this paper is to identify different cases of ethical violation in research and inform and educate researchers to avoid any violations in publication and research ethics. Furthermore, this article will demonstrate how KODISA journals identify and penalize ethical violations and strengthens its publication ethics and practices. Research design, data and methodology – This paper examines different types of ethical violation in publication and research ethics. The paper identifies and analyzes all ethical violations in research and combines them into five general categories. Those five general types of ethical violations are thoroughly examined and discussed. Results – Ethical violations of research occur in various forms at regular intervals; in other words, unethical researchers tend to commit different types of ethical violations repeatedly at same time. The five categories of ethical violation in research are as follows: (1) Arbitrary changes or additions in author(s) happen frequently in thesis/dissertation related publications. (2) Self plagiarism, submitting same work or mixture of previous works with or without using proper citations, also occurs frequently, but the most common type of plagiarism is changing the statistical results and using them to present as the results of the empirical analysis; (3) Translation plagiarism, another ethical violation in publication, is difficult to detect but occurs frequently; (4) Fabrication of data or statistical analysis also occurs frequently. KODISA requires authors to submit the results of the empirical analysis of the paper (the output of the statistical program) to prevent this type of ethical violation; (5) Mashup or aggregator plagiarism, submitting a mix of several different works with or without proper citations without alterations, is very difficult to detect, and KODISA journals consider this type of plagiarism as the worst ethical violation. Conclusions – There are some individual cases of ethical violation in research and publication that could not be included in the five categories presented throughout the paper. KODISA and its editorial office should continue to develop, revise, and strengthen their publication ethics, to learn and share different ways to detect any ethical violations in research and publication, to train and educate its editorial members and researchers, and to analyze and share different cases of ethical violations with the scholarly community

    The mechanism of low-concentration sodium nitroprusside-mediated protection of chondrocyte death

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    Sodium nitroprusside (SNP), a widely used nitric oxide donor, has recently been shown to mediate chondrocyte apoptosis by generating reactive oxygen species, whereas more potent nitric oxide donors do not induce chondrocyte apoptosis. The present study was performed to investigate the protective effect of a low concentration of SNP upon the cytotoxicity of chondrocytes to higher concentrations of SNP, and to elucidate the underlying mechanism. Human osteoarthritis chondrocytes were cultured as monolayers, and first-passage cells were used for the experiments. Chondrocyte death induced by 1 mM SNP was completely inhibited by pretreating with 0.1 mM SNP. This protective effect of SNP was replicated by the guanosine-3',5'κ-cyclic monophosphate analog, DBcGMP. Protection from chondrocyte death conferred by 0.1 mM SNP was mediated by heme oxygenase 1 (HO-1), as was revealed by the increased expression of HO-1 in 0.1 mM SNP pretreated chondrocytes and by the reversal of this protective effect by the HO-1 inhibitor, zinc protoporphyrin. SNP-mediated chondrocyte protection correlated with the downregulation of both extracellular signal-regulated protein kinase 1/2 and p38 kinase activation. SNP at 0.1 mM induced significant NF-κB activation as revealed by electrophoretic mobility shift assays, and the inhibition of NF-κB by MG132 or Bay 11-7082 nullified 0.1 mM SNP-mediated chondrocyte protection. The upregulation of p53 and the downregulation of Bcl-(XL )and Mcl-1 by 1 mM SNP were reversed by 0.1 mM SNP pretreatment at the protein level by western blotting. Our study shows that priming with 0.1 mM SNP confers complete protection against cell death induced by 1 mM SNP in human articular chondrocytes. This protective effect was found to be correlated with the upregulation of both HO-1 and NF-κB and with the concomitant downregulation of both extracellular signal-regulated protein kinase 1/2 and p38 activation

    Leveraging Speaker Embeddings with Adversarial Multi-task Learning for Age Group Classification

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    Recently, researchers have utilized neural network-based speaker embedding techniques in speaker-recognition tasks to identify speakers accurately. However, speaker-discriminative embeddings do not always represent speech features such as age group well. In an embedding model that has been highly trained to capture speaker traits, the task of age group classification is closer to speech information leakage. Hence, to improve age group classification performance, we consider the use of speaker-discriminative embeddings derived from adversarial multi-task learning to align features and reduce the domain discrepancy in age subgroups. In addition, we investigated different types of speaker embeddings to learn and generalize the domain-invariant representations for age groups. Experimental results on the VoxCeleb Enrichment dataset verify the effectiveness of our proposed adaptive adversarial network in multi-objective scenarios and leveraging speaker embeddings for the domain adaptation task

    Vortex-antivortex pair driven magnetization dynamics studied by micromagnetic simulations

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    The magnetization dynamics approaching an equilibrium vortex state from an initial nonequilibrium state under zero magnetic field in a circular shaped Fe disk with thickness of 5 nm and a diameter of 1200 nm were studied. Starting from the initial random configuration of in-plane magnetizations, a great number of vortex and antivortex pairs energetically favorable to form were generated at a lot of nucleation sites. It was found that the sites propagated and then were annihilated by their attractive interactions during the relaxation dynamic process. The study shows that temporal magnetization evolutions can be dominated by the nucleation of the vortex and antivortex pairs, followed by their propagation and annihilation.open222

    Vortex-antivortex assisted magnetization dynamics in a semi-continuous thin-film model system studied by micromagnetic simulations

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    We have studied magnetization M dynamics in a semicontinuous 33-nm -thick Fe model system, which approaches new equilibrium states under various magnetic fields, H=0, -1, -10, and -30 Oe, starting from an initial M configuration of complex microstructures experimentally observed in a real continuous Fe film. Simulation results with H=0 clearly reveal that small needle-shaped domains and ripple structures found in a frozen state of the demagnetized Fe film continue to grow far into a surrounding 180?? domain, and that zigzag folding structures appear through the M dynamic evolution assisted by vortex and antivortex. Furthermore, it is found that many domain walls of a cross-tie type exhibit their dynamic developments under H=-10 and -30 Oe, caused by interactions between vortex and antivortex states. This vortex-antivortex assisted M dynamic evolution offers deeper insights into the comprehensive understanding of the static or dynamic properties of M reversal processes as well as additional features or more details of magnetic microstructures in real continuous films.open141
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