cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7802804.v1
title: Additional file 3: of Discovery and validation of DNA methylation markers for overall survival prognosis in patients with thymic epithelial tumors

description: Table S4. The list of genes transcriptionally affected by methylation of significantly expressed methylation probes within promotor regions. In this table, meaning of the “mean_AB”, “mean_C”, “FC” and “p” is the same asdescribed in “Additional file 1: Table S2”. (XLSX 119 kb)
DOI: 10.6084/m9.figshare.8327093
title: Shrinkage Estimation of Factor Models With Global and Group-Specific Factors

description: This article develops an adaptive group lasso estimator for factor models with both global and group-specific factors. The global factors can affect all variables, whereas the group-specific factors are only allowed to affect the variables within a certain group. We propose a new method to separately identify the spaces spanned by global and group-specific factors, and we develop a new shrinkage estimator that can consistently estimate the factor loadings and determine the number of factors simultaneously. The asymptotic result shows that the proposed estimator can select the true model specification with a probability approaching one. An information criterion is developed to select the optimal tuning parameters in the shrinkage estimation. Monte Carlo simulations confirm our asymptotic theory, and the proposed estimator performs well in finite samples. In an empirical application, we implement the proposed method to a dataset consisting of Eurozone, United States, and United Kingdom macroeconomic variables, and we detect one global factor, one U.S.-specific factor, and one Eurozone-specific factor.
DOI: 10.6084/m9.figshare.8327093.v2
title: Shrinkage Estimation of Factor Models With Global and Group-Specific Factors

description: This article develops an adaptive group lasso estimator for factor models with both global and group-specific factors. The global factors can affect all variables, whereas the group-specific factors are only allowed to affect the variables within a certain group. We propose a new method to separately identify the spaces spanned by global and group-specific factors, and we develop a new shrinkage estimator that can consistently estimate the factor loadings and determine the number of factors simultaneously. The asymptotic result shows that the proposed estimator can select the true model specification with a probability approaching one. An information criterion is developed to select the optimal tuning parameters in the shrinkage estimation. Monte Carlo simulations confirm our asymptotic theory, and the proposed estimator performs well in finite samples. In an empirical application, we implement the proposed method to a dataset consisting of Eurozone, United States, and United Kingdom macroeconomic variables, and we detect one global factor, one U.S.-specific factor, and one Eurozone-specific factor.
DOI: 10.6084/m9.figshare.8327093.v1
title: Shrinkage Estimation of Factor Models With Global and Group-Specific Factors

description: This article develops an adaptive group lasso estimator for factor models with both global and group-specific factors. The global factors can affect all variables, whereas the group-specific factors are only allowed to affect the variables within a certain group. We propose a new method to separately identify the spaces spanned by global and group-specific factors, and we develop a new shrinkage estimator that can consistently estimate the factor loadings and determine the number of factors simultaneously. The asymptotic result shows that the proposed estimator can select the true model specification with a probability approaching one. An information criterion is developed to select the optimal tuning parameters in the shrinkage estimation. Monte Carlo simulations confirm our asymptotic theory, and the proposed estimator performs well in finite samples. In an empirical application, we implement the proposed method to a dataset consisting of Eurozone, United States, and United Kingdom macroeconomic variables, and we detect one global factor, one U.S.-specific factor, and one Eurozone-specific factor.
DOI: 10.6084/m9.figshare.7802813
title: Additional file 5: of Discovery and validation of DNA methylation markers for overall survival prognosis in patients with thymic epithelial tumors

description: Table S5. Summary of results from univariate and multivariable Cox regression for overall survival of probes which potentially affect transcription mRNA. The “Pcg” in this table respectively stands for probabilities for methylation of each probe adjusted for WHO histological type, Masaoka stage based on likelihood ratio test. The “Pt” for probabilities of significance of main effect model including WHO histological type, Masaoka stage and methylation of each probe. The “coeff” for coefficients of each probe in multivariable Cox regression. (XLSX 63 kb)
DOI: 10.6084/m9.figshare.7802813.v1
title: Additional file 5: of Discovery and validation of DNA methylation markers for overall survival prognosis in patients with thymic epithelial tumors

description: Table S5. Summary of results from univariate and multivariable Cox regression for overall survival of probes which potentially affect transcription mRNA. The “Pcg” in this table respectively stands for probabilities for methylation of each probe adjusted for WHO histological type, Masaoka stage based on likelihood ratio test. The “Pt” for probabilities of significance of main effect model including WHO histological type, Masaoka stage and methylation of each probe. The “coeff” for coefficients of each probe in multivariable Cox regression. (XLSX 63 kb)
DOI: 10.5281/zenodo.10724809
title: Park and Lee

description: Data for Park and Lee.
DOI: 10.5281/zenodo.10724810
title: Park and Lee

description: Data for Park and Lee.
DOI: 10.6084/m9.figshare.7802843
title: Additional file 8: of Discovery and validation of DNA methylation markers for overall survival prognosis in patients with thymic epithelial tumors

description: Table S1. List of primers used for pyrosequencing and quantitative RT-PCR. (XLSX 10 kb)
DOI: 10.6084/m9.figshare.7802843.v1
title: Additional file 8: of Discovery and validation of DNA methylation markers for overall survival prognosis in patients with thymic epithelial tumors

description: Table S1. List of primers used for pyrosequencing and quantitative RT-PCR. (XLSX 10 kb)
DOI: 10.6084/m9.figshare.8327156
title: Upregulation of ATG7 attenuates motor neuron dysfunction associated with depletion of TARDBP/TDP-43

description: A shared neuropathological hallmark in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is nuclear clearance and cytoplasmic aggregation of TARDBP/TDP-43 (TAR DNA binding protein). We previously showed that the ability of TARDBP to repress nonconserved cryptic exons was impaired in brains of patients with ALS and FTD, suggesting that its nuclear depletion contributes to neurodegeneration. However, the critical pathways impacted by the failure to repress cryptic exons that may contribute to neurodegeneration remain undefined. Here, we report that transcriptome analysis of TARDBP-deficient neurons revealed downregulation of <i>ATG7</i>, a critical gene required for macroautophagy/autophagy. Mouse and <i>Drosophila</i> models lacking TARDBP/TBPH in motor neurons exhibiting age-dependent neurodegeneration and motor deficits showed reduction of ATG7 and accumulation of SQSTM1/p62 inclusions. Importantly, genetic upregulation of the autophagy pathway improved motor function and survival in TBPH-deficient flies. Together with our observation that ATG7 is reduced in ALS-FTD brain tissues, these findings identify the autophagy pathway as one key effector of nuclear depletion of TARDBP that contributes to neurodegeneration. We thus suggest that the autophagy pathway is a therapeutic target for ALS-FTD and other disorders exhibiting TARDBP pathology. <b>Abbreviations:</b> ALS: amyotrophic lateral sclerosis; ANOVA: analysis of variance; ChAT: choline acetyltransferase; CTSD: cathepsin D; FTD: frontotemporal dementia; LAMP1: lysosomal associated membrane protein 1; NMJ: neuromuscular junction; RBFOX3/NeuN: RNA binding fox-1 homolog 3; SQSTM1: sequestosome 1; TARDBP/TDP-43: TAR DNA binding protein 43.
DOI: 10.6084/m9.figshare.8327156.v1
title: Upregulation of ATG7 Attenuates Motor Neuron Dysfunction Associated with Depletion of TARDBP/TDP-43

description: A shared neuropathological hallmark in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is nuclear clearance and cytoplasmic aggregation of TARDBP/TDP-43 (TAR DNA binding protein). We previously showed that the ability of TARDBP to repress nonconserved cryptic exons was impaired in brains of patients with ALS and FTD, suggesting that its nuclear depletion contributes to neurodegeneration. However, the critical pathways impacted by the failure to repress cryptic exons that may contribute to neurodegeneration remain undefined. Here, we report that transcriptome analysis of TARDBP-deficient neurons revealed downregulation of <i>ATG7</i>, a critical gene required for macroautophagy/autophagy. Mouse and <i>Drosophila</i> models lacking TARDBP/TBPH in motor neurons exhibiting age-dependent neurodegeneration and motor deficits showed reduction of ATG7 and accumulation of SQSTM1/p62 inclusions. Importantly, genetic upregulation of the autophagy pathway improved motor function and survival in TBPH-deficient flies. Together with our observation that ATG7 is reduced in ALS-FTD brain tissues, these findings identify the autophagy pathway as one key effector of nuclear depletion of TARDBP that contributes to neurodegeneration. We thus suggest that the autophagy pathway is a therapeutic target for ALS-FTD and other disorders exhibiting TARDBP pathology.
DOI: 10.6084/m9.figshare.8327156.v3
title: Upregulation of ATG7 attenuates motor neuron dysfunction associated with depletion of TARDBP/TDP-43

description: A shared neuropathological hallmark in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is nuclear clearance and cytoplasmic aggregation of TARDBP/TDP-43 (TAR DNA binding protein). We previously showed that the ability of TARDBP to repress nonconserved cryptic exons was impaired in brains of patients with ALS and FTD, suggesting that its nuclear depletion contributes to neurodegeneration. However, the critical pathways impacted by the failure to repress cryptic exons that may contribute to neurodegeneration remain undefined. Here, we report that transcriptome analysis of TARDBP-deficient neurons revealed downregulation of <i>ATG7</i>, a critical gene required for macroautophagy/autophagy. Mouse and <i>Drosophila</i> models lacking TARDBP/TBPH in motor neurons exhibiting age-dependent neurodegeneration and motor deficits showed reduction of ATG7 and accumulation of SQSTM1/p62 inclusions. Importantly, genetic upregulation of the autophagy pathway improved motor function and survival in TBPH-deficient flies. Together with our observation that ATG7 is reduced in ALS-FTD brain tissues, these findings identify the autophagy pathway as one key effector of nuclear depletion of TARDBP that contributes to neurodegeneration. We thus suggest that the autophagy pathway is a therapeutic target for ALS-FTD and other disorders exhibiting TARDBP pathology. <b>Abbreviations:</b> ALS: amyotrophic lateral sclerosis; ANOVA: analysis of variance; ChAT: choline acetyltransferase; CTSD: cathepsin D; FTD: frontotemporal dementia; LAMP1: lysosomal associated membrane protein 1; NMJ: neuromuscular junction; RBFOX3/NeuN: RNA binding fox-1 homolog 3; SQSTM1: sequestosome 1; TARDBP/TDP-43: TAR DNA binding protein 43.
DOI: 10.6084/m9.figshare.8327156.v2
title: Upregulation of ATG7 attenuates motor neuron dysfunction associated with depletion of TARDBP/TDP-43

description: A shared neuropathological hallmark in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is nuclear clearance and cytoplasmic aggregation of TARDBP/TDP-43 (TAR DNA binding protein). We previously showed that the ability of TARDBP to repress nonconserved cryptic exons was impaired in brains of patients with ALS and FTD, suggesting that its nuclear depletion contributes to neurodegeneration. However, the critical pathways impacted by the failure to repress cryptic exons that may contribute to neurodegeneration remain undefined. Here, we report that transcriptome analysis of TARDBP-deficient neurons revealed downregulation of <i>ATG7</i>, a critical gene required for macroautophagy/autophagy. Mouse and <i>Drosophila</i> models lacking TARDBP/TBPH in motor neurons exhibiting age-dependent neurodegeneration and motor deficits showed reduction of ATG7 and accumulation of SQSTM1/p62 inclusions. Importantly, genetic upregulation of the autophagy pathway improved motor function and survival in TBPH-deficient flies. Together with our observation that ATG7 is reduced in ALS-FTD brain tissues, these findings identify the autophagy pathway as one key effector of nuclear depletion of TARDBP that contributes to neurodegeneration. We thus suggest that the autophagy pathway is a therapeutic target for ALS-FTD and other disorders exhibiting TARDBP pathology. <b>Abbreviations:</b> ALS: amyotrophic lateral sclerosis; ANOVA: analysis of variance; ChAT: choline acetyltransferase; CTSD: cathepsin D; FTD: frontotemporal dementia; LAMP1: lysosomal associated membrane protein 1; NMJ: neuromuscular junction; RBFOX3/NeuN: RNA binding fox-1 homolog 3; SQSTM1: sequestosome 1; TARDBP/TDP-43: TAR DNA binding protein 43.
DOI: 10.6084/m9.figshare.8327159
title: Suboptimal RNA–RNA interaction limits U1 snRNP inhibition of canonical mRNA 3’ processing

description: It is increasingly appreciated that U1 snRNP transcriptomically suppresses the usage of intronic polyadenylation site (PAS) of mRNAs, an outstanding question is why frequently used PASs are not suppressed. Here we found that U1 snRNP could be transiently associated with sequences upstream of actionable PASs in human cells, and RNA–RNA interaction might contribute to the association. By focusing on individual PAS, we showed that the stable assembly of U1 snRNP near PAS might be generally required for U1 inhibition of mRNA 3ʹ processing. Therefore, actionable PASs that often lack optimal U1 snRNP docking site nearby is free from U1 inhibitory effect. Consistently, natural 5ʹ splicing site (5ʹ-SS) is moderately enriched ~250 nt upstream of intronic PASs whose usage is sensitive to functional knockdown of U1 snRNA. Collectively, our results provided an insight into how U1 snRNP selectively inhibits the usage of PASs in a cellular context, and supported a prevailing model that U1 snRNP scans pre-mRNA through RNA–RNA interaction to find a stable interaction site to exercise its function in pre-mRNA processing, including repressing the usage of cryptic PASs.
DOI: 10.6084/m9.figshare.8327159.v1
title: Suboptimal RNA-RNA interaction limits U1 snRNP inhibition of canonical mRNA 3’ processing

description: It is increasingly appreciated that U1 snRNP transcriptomically suppresses the usage of intronic polyadenylation site (PAS) of mRNAs, an outstanding question is why frequently used PASs are not suppressed. Here we found that U1 snRNP could be transiently associated with sequences upstream of actionable PASs in human cells, and RNA-RNA interaction might contribute to the association. By focusing on individual PAS, we showed that the stable assembly of U1 snRNP near PAS might be generally required for U1 inhibition of mRNA 3ʹ processing. Therefore, actionable PASs that often lack optimal U1 snRNP docking site nearby, is free from U1 inhibitory effect. Consistently, natural 5ʹ splicing site (5ʹ-SS) is moderately enriched ~250 nt upstream of intronic PASs whose usage is sensitive to functional knockdown of U1 snRNA. Collectively, our results provided an insight into how U1 snRNP selectively inhibits the usage of PASs in a cellular context, and supported a prevailing model that U1 snRNP scans pre-mRNA through RNA-RNA interaction to find a stable interaction site to exercise its function in pre-mRNA processing, including repressing the usage of cryptic PASs.
DOI: 10.6084/m9.figshare.8327159.v3
title: Suboptimal RNA–RNA interaction limits U1 snRNP inhibition of canonical mRNA 3’ processing

description: It is increasingly appreciated that U1 snRNP transcriptomically suppresses the usage of intronic polyadenylation site (PAS) of mRNAs, an outstanding question is why frequently used PASs are not suppressed. Here we found that U1 snRNP could be transiently associated with sequences upstream of actionable PASs in human cells, and RNA–RNA interaction might contribute to the association. By focusing on individual PAS, we showed that the stable assembly of U1 snRNP near PAS might be generally required for U1 inhibition of mRNA 3ʹ processing. Therefore, actionable PASs that often lack optimal U1 snRNP docking site nearby is free from U1 inhibitory effect. Consistently, natural 5ʹ splicing site (5ʹ-SS) is moderately enriched ~250 nt upstream of intronic PASs whose usage is sensitive to functional knockdown of U1 snRNA. Collectively, our results provided an insight into how U1 snRNP selectively inhibits the usage of PASs in a cellular context, and supported a prevailing model that U1 snRNP scans pre-mRNA through RNA–RNA interaction to find a stable interaction site to exercise its function in pre-mRNA processing, including repressing the usage of cryptic PASs.
DOI: 10.6084/m9.figshare.8327159.v2
title: Suboptimal RNA–RNA interaction limits U1 snRNP inhibition of canonical mRNA 3’ processing

description: It is increasingly appreciated that U1 snRNP transcriptomically suppresses the usage of intronic polyadenylation site (PAS) of mRNAs, an outstanding question is why frequently used PASs are not suppressed. Here we found that U1 snRNP could be transiently associated with sequences upstream of actionable PASs in human cells, and RNA–RNA interaction might contribute to the association. By focusing on individual PAS, we showed that the stable assembly of U1 snRNP near PAS might be generally required for U1 inhibition of mRNA 3ʹ processing. Therefore, actionable PASs that often lack optimal U1 snRNP docking site nearby is free from U1 inhibitory effect. Consistently, natural 5ʹ splicing site (5ʹ-SS) is moderately enriched ~250 nt upstream of intronic PASs whose usage is sensitive to functional knockdown of U1 snRNA. Collectively, our results provided an insight into how U1 snRNP selectively inhibits the usage of PASs in a cellular context, and supported a prevailing model that U1 snRNP scans pre-mRNA through RNA–RNA interaction to find a stable interaction site to exercise its function in pre-mRNA processing, including repressing the usage of cryptic PASs.
DOI: 10.6084/m9.figshare.23531525
title: figure and table from Capturing synchronization with complexity measure of ordinal pattern transition network constructed by crossplot

description: To evaluate the synchronization of bivariate time series has been a hot topic and a number of measures have been proposed. In this work, by introducing the ordinal pattern transition network into the crossplot, a new method for measuring the synchronization of bivariate time series is proposed. After the crossplot been partitioned and coded, the coded partitions are defined as network nodes and a directed weighted network is constructed based on the temporal adjacency of the nodes. The crossplot transition entropy of the network is proposed as an indicator of the synchronization between two time series. To test the characteristics and performance of the method, it is used to analyse the unidirectional coupled Lorentz model and compared it with existing methods. The results showed the new method had the advantages of easy parameter setting, efficiency, robustness, good consistency and suitable for short time series. Finally, EEG data from auditory evoked potential EEG-Biometric dataset are investigated, and some useful and interesting results are obtained.
DOI: 10.6084/m9.figshare.23531525.v1
title: figure and table from Capturing synchronization with complexity measure of ordinal pattern transition network constructed by crossplot

description: To evaluate the synchronization of bivariate time series has been a hot topic and a number of measures have been proposed. In this work, by introducing the ordinal pattern transition network into the crossplot, a new method for measuring the synchronization of bivariate time series is proposed. After the crossplot been partitioned and coded, the coded partitions are defined as network nodes and a directed weighted network is constructed based on the temporal adjacency of the nodes. The crossplot transition entropy of the network is proposed as an indicator of the synchronization between two time series. To test the characteristics and performance of the method, it is used to analyse the unidirectional coupled Lorentz model and compared it with existing methods. The results showed the new method had the advantages of easy parameter setting, efficiency, robustness, good consistency and suitable for short time series. Finally, EEG data from auditory evoked potential EEG-Biometric dataset are investigated, and some useful and interesting results are obtained.
DOI: 10.6084/m9.figshare.9900059
title: Atomization Characteristics of Droplet and Morphologies of Arc Sprayed Ni-Al Particles and Composition Coatings

description: Droplet atomization characteristics and its morphology in twin-wire arc sprayed (TWAS) Ni-Al were explored in depth. Both numerical model and theoretical method were built for calculating the process of the droplet deformation and breakup in air flow, which based on the standard k-ε model and the volume of fluid (VOF) dual-phase flow model. The atomization characteristics of double droplets and three droplets were also studied in the atomization process by simulation. The micro structure and the morphology of the composite coatings were analyzed by SEM and TEM. The experimental results indicate that TWAS droplets are the process of explosive breakup or two steps breakup. Morphology of the TWAS prepared Ni-20wt.%Al and Ni-5wt.%Al particles was accordingly characterized by SEM. The phase compositions of the Ni-Al particles were obtained by EDS. By testing the velocity of sprayed particles, the change rule of particles with spray pressure was obtained. Ni twins are discovered in the Ni-Al coating due to rapid cooling in TWAS process.
DOI: 10.6084/m9.figshare.9900059.v1
title: Atomization Characteristics of Droplet and Morphologies of Arc Sprayed Ni-Al Particles and Composition Coatings

description: Droplet atomization characteristics and its morphology in twin-wire arc sprayed (TWAS) Ni-Al were explored in depth. Both numerical model and theoretical method were built for calculating the process of the droplet deformation and breakup in air flow, which based on the standard k-ε model and the volume of fluid (VOF) dual-phase flow model. The atomization characteristics of double droplets and three droplets were also studied in the atomization process by simulation. The micro structure and the morphology of the composite coatings were analyzed by SEM and TEM. The experimental results indicate that TWAS droplets are the process of explosive breakup or two steps breakup. Morphology of the TWAS prepared Ni-20wt.%Al and Ni-5wt.%Al particles was accordingly characterized by SEM. The phase compositions of the Ni-Al particles were obtained by EDS. By testing the velocity of sprayed particles, the change rule of particles with spray pressure was obtained. Ni twins are discovered in the Ni-Al coating due to rapid cooling in TWAS process.