cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.23866868.v2
title: Change Point Detection in Dynamic Networks via Regularized Tensor Decomposition

description: Dynamic network captures time-varying interactions among multiple entities at different time points, and detecting its structural change points is of central interest. This article proposes a novel method for detecting change points in dynamic networks by fully exploiting the latent network structure. The proposed method builds upon a tensor-based embedding model, which models the time-varying network heterogeneity through an embedding matrix. A fused lasso penalty is equipped with the tensor decomposition formulation to estimate the embedding matrix and a power update algorithm is developed to tackle the resultant optimization task. The error bound of the obtained estimated embedding matrices is established without incurring the computational-statistical gap. The proposed method also produces a set of estimated change points, which, coupled with a simple screening procedure, assures asymptotic consistency in change point detection under much milder assumptions. Various numerical experiments on both synthetic and real datasets also support its advantage. Supplementary materials for this article are available online.
DOI: 10.6084/m9.figshare.23866868.v1
title: Change point detection in dynamic networks via regularized tensor decomposition

description: Dynamic network captures time-varying interactions among multiple entities at different time points, and detecting its structural change points is of central interest. This paper proposes a novel method for detecting change points in dynamic networks by fully exploiting the latent network structure. The proposed method builds upon a tensor-based embedding model, which models the time-varying network heterogeneity through an embedding matrix. A fused lasso penalty is equipped with the tensor decomposition formulation to estimate the embedding matrix and a power update algorithm is developed to tackle the resultant optimization task. The error bound of the obtained estimated embedding matrices is established without incurring the computational-statistical gap. The proposed method also produces a set of estimated change points, which, coupled with a simple screening procedure, assures asymptotic consistency in change point detection under much milder assumptions. Various numerical experiments on both synthetic and real datasets also support its advantage.
DOI: 10.6084/m9.figshare.21769871
title: Relationship between Antithrombin III Activity and Mortality in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease

description: We aimed to explore the role of antithrombin III (AT-III) activity in diagnosing patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and chronic bronchitis, and its relationship with all-cause mortality of AECOPD patients. We performed univariate and multivariate Cox regression analyses of the factors determining all-cause mortality. We recruited 279 patients with AECOPD and 91 with chronic bronchitis. On admission, patients with AECOPD had lower AT-III activity (80.7 vs. 86.35%, <i>p</i> = 0.002) and higher neutrophil percentages (70.12 vs. 66.40%, <i>p</i> = 0.02) than those with chronic bronchitis. The patients who died were older (78 vs. 73 years, <i>p</i> &lt; 0.001); had higher CRP (39.05 vs. 5.65 mg/L, <i>p</i> &lt; 0.001), D-dimer (1.72 vs. 0.46 mg/L, <i>p</i> &lt; 0.001), FIB (3.56 vs. 3.05 g/L, <i>p</i> = 0.01) levels; and exhibited lower AT-III activity (71.29 vs. 82.94%, <i>p</i> &lt; 0.001) than the survivors. The AT-III area under the receiver operating characteristic curve for predicting COPD all-cause mortality was 0.75 (<i>p</i> &lt; 0.001), optimal cutoff point 79.75%, sensitivity 86.8%, and specificity 57.1%. Multivariate Cox regression analyses showed that increased levels of CRP (HR = 1.005, <i>p</i> = 0.02), D-dimer (HR = 1.17, <i>p</i> = 0.01), WBC count (HR = 1.11, <i>p</i> = 0.002), and reduced AT-III activity (HR = 0.97, <i>p</i> = 0.02) were independent prognostic factors for all-cause mortality. Patients with AT-III ≤ 79.75% were 4.52 times (<i>p</i> = 0.001) more likely to die than those with AT-III &gt; 79.75%. AT-III activity was lower in patients with AECOPD than in those with chronic bronchitis and is potentially useful as an independent predictor of all-cause mortality in patients with AECOPD: reduced AT-III activity and increased CRP and D-dimer levels indicate a higher risk of all-cause mortality.
DOI: 10.6084/m9.figshare.21769871.v1
title: Relationship between Antithrombin III Activity and Mortality in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease

description: We aimed to explore the role of antithrombin III (AT-III) activity in diagnosing patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and chronic bronchitis, and its relationship with all-cause mortality of AECOPD patients. We performed univariate and multivariate Cox regression analyses of the factors determining all-cause mortality. We recruited 279 patients with AECOPD and 91 with chronic bronchitis. On admission, patients with AECOPD had lower AT-III activity (80.7 vs. 86.35%, <i>p</i> = 0.002) and higher neutrophil percentages (70.12 vs. 66.40%, <i>p</i> = 0.02) than those with chronic bronchitis. The patients who died were older (78 vs. 73 years, <i>p</i> &lt; 0.001); had higher CRP (39.05 vs. 5.65 mg/L, <i>p</i> &lt; 0.001), D-dimer (1.72 vs. 0.46 mg/L, <i>p</i> &lt; 0.001), FIB (3.56 vs. 3.05 g/L, <i>p</i> = 0.01) levels; and exhibited lower AT-III activity (71.29 vs. 82.94%, <i>p</i> &lt; 0.001) than the survivors. The AT-III area under the receiver operating characteristic curve for predicting COPD all-cause mortality was 0.75 (<i>p</i> &lt; 0.001), optimal cutoff point 79.75%, sensitivity 86.8%, and specificity 57.1%. Multivariate Cox regression analyses showed that increased levels of CRP (HR = 1.005, <i>p</i> = 0.02), D-dimer (HR = 1.17, <i>p</i> = 0.01), WBC count (HR = 1.11, <i>p</i> = 0.002), and reduced AT-III activity (HR = 0.97, <i>p</i> = 0.02) were independent prognostic factors for all-cause mortality. Patients with AT-III ≤ 79.75% were 4.52 times (<i>p</i> = 0.001) more likely to die than those with AT-III &gt; 79.75%. AT-III activity was lower in patients with AECOPD than in those with chronic bronchitis and is potentially useful as an independent predictor of all-cause mortality in patients with AECOPD: reduced AT-III activity and increased CRP and D-dimer levels indicate a higher risk of all-cause mortality.
DOI: 10.6084/m9.figshare.12332507
title: Additional file 2 of Species richness, forest types and regeneration of Schima in the subtropical forest ecosystem of Yunnan, southwestern China

description: Additional file 2.Supplementary Table S2. DBH-classes of major species (RIV ≥ 1.5%) of each secondary forest type.
DOI: 10.6084/m9.figshare.12332507.v1
title: Additional file 2 of Species richness, forest types and regeneration of Schima in the subtropical forest ecosystem of Yunnan, southwestern China

description: Additional file 2.Supplementary Table S2. DBH-classes of major species (RIV ≥ 1.5%) of each secondary forest type.
DOI: 10.6084/m9.figshare.12332501
title: Additional file 1 of Species richness, forest types and regeneration of Schima in the subtropical forest ecosystem of Yunnan, southwestern China

description: Additional file 1.Supplementary Table S1. DBH-classes of species (IV ≥ 1.5%) of each primary forest type.
DOI: 10.6084/m9.figshare.12332501.v1
title: Additional file 1 of Species richness, forest types and regeneration of Schima in the subtropical forest ecosystem of Yunnan, southwestern China

description: Additional file 1.Supplementary Table S1. DBH-classes of species (IV ≥ 1.5%) of each primary forest type.
DOI: 10.6084/m9.figshare.19672983
title: Circular <i>GOLPH3</i> RNA exerts oncogenic effects <i>in vitro</i> by regulating the miRNA-1299/LIF axis in oral squamous cell carcinoma

description: Circular RNAs, which are a novel subclass of noncoding RNAs, are reported to be involved in various biological processes. Aberrant expression of circular RNAs may promote cancer progression. The function of circular <i>GOLPH3</i> RNA (circGOLPH3) in oral squamous cell carcinoma (OSCC) is unclear. In this study, the circGOLPH3 levels in OSCC cell lines were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Gain-of-function and loss-of-function experiments were performed to evaluate the roles of circGOLPH3 in OSCC. Cell counting kit 8, migration, and invasion assays were performed to determine the functions of circGOLPH3. The mechanism of circGOLPH3 in OSCC was investigated using qRT-PCR, western blotting, luciferase activity, and RNA pull-down analyses. Furthermore, the function of circGOLPH3 <i>in vivo</i> was evaluated. circGOLPH3 derived from <i>GOLPH3</i> was mainly localized to the cytoplasm and exhibited high stability. The expression of circGOLPH3 was upregulated in OSCC cells. circGOLPH3 promoted the growth of OSCC <i>in vitro</i> and <i>in vivo</i>. Additionally, circGOLPH3 upregulated OSCC cell migration and invasion. Mechanistically, circGOLPH3 functioned as a microRNA sponge and downregulated miR-1299 expression. miR-1299 downregulated the expression of <i>LIF</i> by targeting its 3’-untranslated region. Inhibition of the circGOLPH3/miR-1299/LIF axis suppressed the growth, migration, and invasion of OSCC cells. These findings indicate that the circGOLPH3/miR-1299/LIF axis promotes OSCC cell growth, migration, and invasion and that this axis is a potential therapeutic target for OSCC.
DOI: 10.6084/m9.figshare.11284487
title: <i>ybjX</i> mutation regulated avian pathogenic <i>Escherichia coli</i> pathogenicity though stress-resistance pathway

description: <i>ybjX</i> gene mutation decreased the pathogenicity of the avian pathogenic <i>Escherichia coli</i> strain, AE17. However, the associated regulatory mechanism of <i>ybjX</i> remains unknown. In this study, we examined the bactericidal activity of chicken serum and blood, as well as bacterial survival in HD11 macrophages. We compared the transcriptome of <i>ybjX</i> mutations with those of the wild strain and studied the effects of <i>ybjX</i> on miRNA expression in the spleen. Our findings revealed that the mutant strain, Δ<i>ybjX</i>, had a lower resistance to chicken serum and blood, as well as lower bacterial survival in HD11 macrophages than AE17. RNA sequencing analyses showed that the <i>ybjX</i> mutation reduced stress resistance by down-regulating mRNAs in metabolic pathways. Infection with the <i>ybjX</i> mutant strain caused changes in the splenic miRNA profile. We verified Kelch repeat and BTB domain-containing protein 11 to be the target of miR-133b. Together, these findings suggest that the <i>ybjX</i> mutation reduces serum, blood, and environmental stress resistance by down-regulating the mRNA in metabolic pathways.
DOI: 10.6084/m9.figshare.11284487.v1
title: <i>ybjX</i> mutation regulated avian pathogenic <i>Escherichia coli</i> pathogenicity though stress-resistance pathway

description: <i>ybjX</i> gene mutation decreased the pathogenicity of the avian pathogenic <i>Escherichia coli</i> strain, AE17. However, the associated regulatory mechanism of <i>ybjX</i> remains unknown. In this study, we examined the bactericidal activity of chicken serum and blood, as well as bacterial survival in HD11 macrophages. We compared the transcriptome of <i>ybjX</i> mutations with those of the wild strain and studied the effects of <i>ybjX</i> on miRNA expression in the spleen. Our findings revealed that the mutant strain, Δ<i>ybjX</i>, had a lower resistance to chicken serum and blood, as well as lower bacterial survival in HD11 macrophages than AE17. RNA sequencing analyses showed that the <i>ybjX</i> mutation reduced stress resistance by down-regulating mRNAs in metabolic pathways. Infection with the <i>ybjX</i> mutant strain caused changes in the splenic miRNA profile. We verified Kelch repeat and BTB domain-containing protein 11 to be the target of miR-133b. Together, these findings suggest that the <i>ybjX</i> mutation reduces serum, blood, and environmental stress resistance by down-regulating the mRNA in metabolic pathways.
DOI: 10.6084/m9.figshare.22294666
title: An interprovincial input–output database distinguishing firm ownership

description: An interprovincial input–output database distinguishing firm ownership in China from 1997 to 2017. Including the IPIO tables, related files and codes.
DOI: 10.6084/m9.figshare.19672983.v1
title: Circular <i>GOLPH3</i> RNA exerts oncogenic effects <i>in vitro</i> by regulating the miRNA-1299/LIF axis in oral squamous cell carcinoma

description: Circular RNAs, which are a novel subclass of noncoding RNAs, are reported to be involved in various biological processes. Aberrant expression of circular RNAs may promote cancer progression. The function of circular <i>GOLPH3</i> RNA (circGOLPH3) in oral squamous cell carcinoma (OSCC) is unclear. In this study, the circGOLPH3 levels in OSCC cell lines were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Gain-of-function and loss-of-function experiments were performed to evaluate the roles of circGOLPH3 in OSCC. Cell counting kit 8, migration, and invasion assays were performed to determine the functions of circGOLPH3. The mechanism of circGOLPH3 in OSCC was investigated using qRT-PCR, western blotting, luciferase activity, and RNA pull-down analyses. Furthermore, the function of circGOLPH3 <i>in vivo</i> was evaluated. circGOLPH3 derived from <i>GOLPH3</i> was mainly localized to the cytoplasm and exhibited high stability. The expression of circGOLPH3 was upregulated in OSCC cells. circGOLPH3 promoted the growth of OSCC <i>in vitro</i> and <i>in vivo</i>. Additionally, circGOLPH3 upregulated OSCC cell migration and invasion. Mechanistically, circGOLPH3 functioned as a microRNA sponge and downregulated miR-1299 expression. miR-1299 downregulated the expression of <i>LIF</i> by targeting its 3’-untranslated region. Inhibition of the circGOLPH3/miR-1299/LIF axis suppressed the growth, migration, and invasion of OSCC cells. These findings indicate that the circGOLPH3/miR-1299/LIF axis promotes OSCC cell growth, migration, and invasion and that this axis is a potential therapeutic target for OSCC.
DOI: 10.25387/g3.8138951
title: Supplementary Material for Wang et al., 2019

description: Table S1 contains copy numbers and distribution patterns of homologs of key enzymes involved in the metabolism of five types of energy reserves in bacteria. Table S2 contains information about homologous sequences of the fungal enzyme PDAT in bacteria based on HMM screening.<br>
DOI: 10.25387/g3.8138951.v1
title: Supplementary Material for Wang et al., 2019

description: Table S1 contains copy numbers and distribution patterns of homologs of key enzymes involved in the metabolism of five types of energy reserves in bacteria. Table S2 contains information about homologous sequences of the fungal enzyme PDAT in bacteria based on HMM screening.<br>
DOI: 10.6084/m9.figshare.1323270
title: Model-Based Sampling Design for Multivariate Geostatistics

description: The quality of inferences made from geostatistical data is affected significantly by the spatial locations, or <i>design</i>, of the sites that are sampled. A large body of published work exists on sampling design for univariate geostatistics, but not for multivariate geostatistics. This article considers multivariate spatial sampling design based on criteria targeted at classical co-kriging (prediction with known covariance parameters), estimation of covariance (including cross-covariance) parameters, and empirical co-kriging (prediction with estimated covariance parameters). Through a combination of analytical results and examples, we investigate the characteristics of optimal designs with respect to each criterion, addressing in particular the design’s degree of collocation. We also consider the robustness of the optimal design to the strength of spatial correlation and cross-correlation; the effects of smoothness and/or separability of the sampled process on the optimal design; the relationship between optimal designs for the multivariate problems considered here and univariate problems considered previously; and the efficiency of optimal collocated designs. One key finding is that optimal collocated designs are highly efficient in many cases. Supplementary materials are available online.
DOI: 10.6084/m9.figshare.1323270.v1
title: Model-Based Sampling Design for Multivariate Geostatistics

description: The quality of inferences made from geostatistical data is affected significantly by the spatial locations, or <i>design</i>, of the sites that are sampled. A large body of published work exists on sampling design for univariate geostatistics, but not for multivariate geostatistics. This article considers multivariate spatial sampling design based on criteria targeted at classical co-kriging (prediction with known covariance parameters), estimation of covariance (including cross-covariance) parameters, and empirical co-kriging (prediction with estimated covariance parameters). Through a combination of analytical results and examples, we investigate the characteristics of optimal designs with respect to each criterion, addressing in particular the design’s degree of collocation. We also consider the robustness of the optimal design to the strength of spatial correlation and cross-correlation; the effects of smoothness and/or separability of the sampled process on the optimal design; the relationship between optimal designs for the multivariate problems considered here and univariate problems considered previously; and the efficiency of optimal collocated designs. One key finding is that optimal collocated designs are highly efficient in many cases. Supplementary materials are available online.
DOI: 10.6084/m9.figshare.19673523
title: Caffeic acid dimethyl ether alleviates alcohol-induced hepatic steatosis via microRNA-378b-mediated CaMKK2-AMPK pathway

description: Alcoholic liver disease (ALD), with its increasing morbidity and mortality, has seriously and extensively affected the health of people worldwide. Caffeic Acid Dimethyl Ether (CADE) significantly inhibits alcohol-induced hepatic steatosis <i>in vivo</i> through AMP-activated protein kinase (AMPK) pathway, but its in-depth mechanism remains unclear. This work aimed to clarify further mechanism of CADE in improving hepatic lipid accumulation in ALD through the microRNA-378b (miR-378b)-mediated Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2)-AMPK signaling pathway. Here, we reported that the hepatic or serum triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), and aspartate transaminase (AST) levels were sharply escalated by ethanol while prominently decreased by CADE. Ethanol sharply up-regulated miR-378b expression while CADE effectively prevented the elevation of miR-378b <i>in vivo</i>. And treatment of CADE surely increased mRNA and protein expression of CaMKK2 as a kinase of AMPK and reduced lipid accumulation in the livers of alcohol-fed C57BL/6 mice. MiR-378b escalation exacerbated hepatic steatosis and inhibited CaMKK2-AMPK signaling, while miR-378b deficiency alleviated lipid accumulation and activated the CaMKK2 cascade. Furthermore, CADE alleviated the lipid deposition and reversed the disorder of CaMKK2-AMPK signaling pathway induced by miR-378b over-expression. However, knockdown of miR-378b eliminated the beneficial effect of CADE on lipid metabolism. In brief, our results showed that CADE ultimately improved hepatic lipid deposition by regulating the CaMKK2-AMPK signaling pathway through miR-378b.
DOI: 10.6084/m9.figshare.19673523.v1
title: Caffeic acid dimethyl ether alleviates alcohol-induced hepatic steatosis via microRNA-378b-mediated CaMKK2-AMPK pathway

description: Alcoholic liver disease (ALD), with its increasing morbidity and mortality, has seriously and extensively affected the health of people worldwide. Caffeic Acid Dimethyl Ether (CADE) significantly inhibits alcohol-induced hepatic steatosis <i>in vivo</i> through AMP-activated protein kinase (AMPK) pathway, but its in-depth mechanism remains unclear. This work aimed to clarify further mechanism of CADE in improving hepatic lipid accumulation in ALD through the microRNA-378b (miR-378b)-mediated Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2)-AMPK signaling pathway. Here, we reported that the hepatic or serum triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), and aspartate transaminase (AST) levels were sharply escalated by ethanol while prominently decreased by CADE. Ethanol sharply up-regulated miR-378b expression while CADE effectively prevented the elevation of miR-378b <i>in vivo</i>. And treatment of CADE surely increased mRNA and protein expression of CaMKK2 as a kinase of AMPK and reduced lipid accumulation in the livers of alcohol-fed C57BL/6 mice. MiR-378b escalation exacerbated hepatic steatosis and inhibited CaMKK2-AMPK signaling, while miR-378b deficiency alleviated lipid accumulation and activated the CaMKK2 cascade. Furthermore, CADE alleviated the lipid deposition and reversed the disorder of CaMKK2-AMPK signaling pathway induced by miR-378b over-expression. However, knockdown of miR-378b eliminated the beneficial effect of CADE on lipid metabolism. In brief, our results showed that CADE ultimately improved hepatic lipid deposition by regulating the CaMKK2-AMPK signaling pathway through miR-378b.
DOI: 10.6084/m9.figshare.8139359
title: IPA scaffold files after selecting for mitochondrial proteins by the Scaffold software

description: IPA Proteomic Scaffold files of cFCMs 40 and 115 days vs 12 days, dFCMs 39 and 105 days Vs 12 days and Adult (90 days) vs neonate (1 day) selected for mitochondrial proteins by the Scaffold software.
DOI: 10.6084/m9.figshare.12858176
title: Protein Biomarkers and Risk Scores in Pulmonary Arterial Hypertension Associated with Ventricular Septal Defect: Integration of Multi-Omics and Validation

description: The molecular mechanisms underlying pulmonary arterial hypertension (PAH) in congenital ventricular septal defects (VSD) are unclear. We aimed to reveal molecular pathways and potential biomarkers by multi-omics analysis in VSD-PAH. Plasma from 160 children, including 120 VSD patients with/without PAH and 40 healthy children was studied by integrated proteomics, metabolomics, and bioinformatics analyses. Proteomics (iTRAQ) identified 107 differential proteins (DPs) between patients with/without PAH including significantly increased ADIPO, DBH, ANPEP, TRF1, GP1BA and decreased GNAS in VSD-PAH. Metabolomics discovered 191 differential metabolites between patients with/without PAH including elevation of 5-HT, taurine, creatine, sarcosine, and 2-oxobutanoate and decrease of vanillylmandelic acid, 3,4-dihydroxymandelate, 15-Keto-PGF2𝛼, fructose-6-phosphate , L-glutamine, dehydroascorbate, hydroxypyruvate, threonine, L-cystine, and 1-aminocyclopropane-1-carboxylate. The DPs differential proteins were validated in a new cohort of patients (N=80). Integrated analyses identified key pathways including cAMP, ECM-receptor interaction, AMPK, HIF-1, PI3K-Akt signaling pathways, and amino acid metabolisms. Increased plasma protein levels of DBH, ADIPO, and ANPEP were found to be independently associated with the occurrence of PAH with a new total risk score from these three proteins developed for clinical diagnosis. In this integrated multi-omics analysis in VSD-PAH patients, we have for the first time found that VSD-PAH patients present important differential proteins, metabolites, and key pathways. We have developed a total-risk-score (based on the plasma concentration of DBH, ANPEP and ADIPO) as predictor of development of PAH in CHD-VSD patients. Therefore, these proteins may be used as biomarkers and the new total-risk-score has significant clinical implications in the diagnosis of PAH.
DOI: 10.34740/kaggle/dsv/7630293
title: Global Genomic Neurofibromatosis Neoplasia
DOI: 10.34740/kaggle/dsv/7029326
title: Wikipedia Text Corpus