cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5884930.v1
title: Dataset for: Identification of cancer-related potential biomarkers based on lncRNA-pseudogene-mRNA competitive networks

description: Accumulating evidences indicate that mRNAs and ncRNAs act as competitive endogenous RNAs and play a key role in tumorigenesis. However, the complex competitive relationship among genes remains unknown. In our study, the lncRNAs, pseudogenes and mRNAs that compete with the common miRNAs are defined as lncRNA-pseudogene-mRNA competitive triples. We find some candidate ceRNAs, modules and triples are related with cancers and can significantly divide patients into high-risk and low-risk groups, and thus they may serve as potential cancer biomarkers. In total, the work systematically analyzes the association between competitive triples and cancer, which will provide a reference for deep understanding of cancer progression.
DOI: 10.6084/m9.figshare.5883124
title: Revisiting the minimum set cover, the maximal coverage models and a maximum benefit area selection model to make climate-change-concerned conservation plans effective (MPS file generators)

description: A set of tools that produce mps files of various conservation area prioritization models developed to handle climate chnage impacts over species range shifts.<br>
DOI: 10.6084/m9.figshare.5883124.v1
title: Revisiting the minimum set cover, the maximal coverage models and a maximum benefit area selection model to make climate-change-concerned conservation plans effective (MPS file generators)

description: A set of tools that produce mps files of various conservation area prioritization models developed to handle climate chnage impacts over species range shifts.<br>
DOI: 10.6084/m9.figshare.5882818
title: Published research on flipped learning 2000-2018

description: This data set shows the number of peer-reviewed published articles from the ERIC database, with one of the terms "flipped learning", "flipped classroom", or "inverted classroom" in either the title or abstract. The data include works published between 2000 and 2018 inclusively.
DOI: 10.6084/m9.figshare.5882818.v1
title: Published research on flipped learning 2000-2017

description: This data set shows the number of peer-reviewed published articles from the ERIC database, with one of the terms "flipped learning", "flipped classroom", or "inverted classroom" in either the title or abstract. The data include works published between 2000 and 2017 inclusively.
DOI: 10.6084/m9.figshare.5882818.v2
title: Published research on flipped learning 2000-2017

description: This data set shows the number of peer-reviewed published articles from the ERIC database, with one of the terms "flipped learning", "flipped classroom", or "inverted classroom" in either the title or abstract. The data include works published between 2000 and 2017 inclusively.
DOI: 10.6084/m9.figshare.5882803
title: Plant species area relationships are determined by evenness, cover and aggregation in drylands worldwide

description: 1.Data file from all sites that were analyzed. 2. Metadata file with explanation of all variables3. R code used to analyze the data
DOI: 10.6084/m9.figshare.5882803.v1
title: Plant species area relationships are determined by evenness, cover and aggregation in drylands worldwide

description: 1.Data file from all sites that were analyzed. 2. Metadata file with explanation of all variables3. R code used to analyze the data
DOI: 10.6084/m9.figshare.5882635
title: Code from: The interplay between movement, morphology and dispersal in Tetrahymena ciliates

description: This fileset contains R scripts to reproduce the analyses and figures from the manuscript.
DOI: 10.6084/m9.figshare.5882551
title: Effect of oxygen therapy on chest pain in patients with ST elevation myocardial infarction: results from the randomized SOCCER trial

description: <i>Objective.</i> Oxygen (O<sub>2</sub>) have been a cornerstone in the treatment of acute myocardial infarction. Studies have been inconclusive regarding the cardiovascular and analgesic effects of oxygen in these patients. In the SOCCER trial, we compared the effects of oxygen treatment versus room air in patients with ST-elevation myocardial infarction (STEMI). There was no difference in myocardial salvage index or infarct size assessed with cardiac magnetic resonance imaging. In the present subanalysis, we wanted to evaluate the effect of O<sub>2</sub> on chest pain in patients with STEMI. <i>Design.</i> Normoxic patients with first time STEMI were randomized in the ambulance to standard care with 10 l/min O<sub>2</sub> or room air until the end of the percutaneous coronary intervention (PCI). The ambulance personnel noted the patients´ chest pain on a visual analog scale (VAS; 1-10) before randomization and after the transport but before the start of the PCI, and also registered the amount of morphine given. <i>Results.</i> 160 patients were randomized to O<sub>2</sub> (<i>n =</i> 85) or room air (<i>n =</i> 75). The O<sub>2</sub> group had a higher median VAS at randomization than the air group (7.0 ± 2.3 vs 6.0 ± 2.9; <i>p</i> = .02) and also received a higher median total dose of morphine (5.0 mg ± 4.4 vs 4.0 mg ± 3.7; <i>p</i> = .02). There was no difference between the O<sub>2</sub> and air groups in VAS at the start of the PCI (4.0 ± 2.4 vs 3.0 ± 2.5; <i>p</i> = .05) or in the median VAS decrease from randomization to the start of the PCI (−2.0 ± 2.2 vs −1.0 ± 2.9; <i>p</i> = .18). <i>Conclusion.</i> Taken together with previously published data, these results do not support a significant analgesic effect of oxygen in patients with STEMI. <b>European Clinical Trials Database (EudraCT):</b> 2011-001452-11. <b>ClinicalTrials.gov Identifier:</b> NCT01423929
DOI: 10.6084/m9.figshare.5882551.v1
title: Effect of oxygen therapy on chest pain in patients with ST elevation myocardial infarction: results from the randomized SOCCER trial

description: <i>Objective.</i> Oxygen (O<sub>2</sub>) have been a cornerstone in the treatment of acute myocardial infarction. Studies have been inconclusive regarding the cardiovascular and analgesic effects of oxygen in these patients. In the SOCCER trial, we compared the effects of oxygen treatment versus room air in patients with ST-elevation myocardial infarction (STEMI). There was no difference in myocardial salvage index or infarct size assessed with cardiac magnetic resonance imaging. In the present subanalysis, we wanted to evaluate the effect of O<sub>2</sub> on chest pain in patients with STEMI. <i>Design.</i> Normoxic patients with first time STEMI were randomized in the ambulance to standard care with 10 l/min O<sub>2</sub> or room air until the end of the percutaneous coronary intervention (PCI). The ambulance personnel noted the patients´ chest pain on a visual analog scale (VAS; 1-10) before randomization and after the transport but before the start of the PCI, and also registered the amount of morphine given. <i>Results.</i> 160 patients were randomized to O<sub>2</sub> (<i>n =</i> 85) or room air (<i>n =</i> 75). The O<sub>2</sub> group had a higher median VAS at randomization than the air group (7.0 ± 2.3 vs 6.0 ± 2.9; <i>p</i> = .02) and also received a higher median total dose of morphine (5.0 mg ± 4.4 vs 4.0 mg ± 3.7; <i>p</i> = .02). There was no difference between the O<sub>2</sub> and air groups in VAS at the start of the PCI (4.0 ± 2.4 vs 3.0 ± 2.5; <i>p</i> = .05) or in the median VAS decrease from randomization to the start of the PCI (−2.0 ± 2.2 vs −1.0 ± 2.9; <i>p</i> = .18). <i>Conclusion.</i> Taken together with previously published data, these results do not support a significant analgesic effect of oxygen in patients with STEMI. <b>European Clinical Trials Database (EudraCT):</b> 2011-001452-11. <b>ClinicalTrials.gov Identifier:</b> NCT01423929
DOI: 10.6084/m9.figshare.5882530
title: Data from: The interplay between movement, morphology and dispersal in Tetrahymena ciliates

description: Dataset to reproduce Fig. 1:smoove_compare_model_fit.csv<br><br>Datasets to reproduce ANOVA analyses and Fig. 2:Activity_mov_all_strains.csvMovement_parameters_all_strains.csv<br>Dataset to reproduce figure 3 and linear models/model selection:movement_morph_correlations.csvmvt_morph_differences_within.csv<br>Movement_parameters_all_strains.csv<br><br>Dataset to reproduce figure 4:dispersal.csv<br>Datasets for model selection:Movement_parameters_all_strains.csv<br>disp_mov_act_analysis.csv<br>Dataset to reproduce Fig. S3:<br>approximate_vs_exact_speed_estimates.csv<br><br>Dataset to reproduce Fig. S4:<br>smoove_best_model_fit.csv<br><br>Dataset to reproduce Fig. S5:<br>mvt_morph_differences_within.csv<br><br>
DOI: 10.6084/m9.figshare.5882530.v1
title: Data from: The interplay between movement, morphology and dispersal in Tetrahymena ciliates

description: Dataset to reproduce Fig. 1:smoove_compare_model_fit.csv<br><br>Datasets to reproduce ANOVA analyses and Fig. 2:Activity_mov_all_strains.csvMovement_parameters_all_strains.csv<br>Dataset to reproduce figure 3 and linear models/model selection:movement_morph_correlations.csvmvt_morph_differences_within.csv<br>Movement_parameters_all_strains.csv<br><br>Dataset to reproduce figure 4:dispersal.csv<br>Datasets for model selection:Movement_parameters_all_strains.csv<br>disp_mov_act_analysis.csv<br>Dataset to reproduce Fig. S3:<br>approximate_vs_exact_speed_estimates.csv<br><br>Dataset to reproduce Fig. S4:<br>smoove_best_model_fit.csv<br><br>Dataset to reproduce Fig. S5:<br>mvt_morph_differences_within.csv<br><br>
DOI: 10.6084/m9.figshare.5882512
title: Supplementary Material for: Cyclic Mechanical Stretch Induced Smooth Muscle Cell Changes in Cerebral Aneurysm Progress by Reducing Collagen Type IV and Collagen Type VI Levels

description: <b><i>Background/Aims:</i></b> Cerebral aneurysm growth is characterized by continuous structural weakness of local smooth muscle cells, though the mechanism is unclear. In this study, we examine protein changes in cerebral aneurysm and human brain vascular smooth muscle cells after cyclic mechanical stretch. We further explore the relationship between the smooth muscle cell changes and reductions in the levels of collagen types IV and VI. <b><i>Methods:</i></b> Saccular cerebral aneurysms (n=10) were collected, and temporal artery samples were used as controls. Quantitative proteomics were analyzed and histopathological changes were examined. Smooth muscle cells were cultured in a flexible silicone chamber and subjected to 15% cyclic mechanical stretch. The effect of stretch on the cell viability, function, gene and protein expression were further studied for the understanding the molecular mechanism of aneurysm development. <b><i>Results:</i></b> Proteomics analysis revealed 92 proteins with increased expression and 88 proteins with decreased expression compared to the controls (<i>p</i>&lt;0.05). KEGG pathway analysis showed that the change in focal adhesion and extracellular matrix-receptor interaction, suggesting the involvement of collagen type IV and VI. The aneurysm tissue exhibited fewer smooth muscle cells and lower levels of collagen type IV and VI. Human brain vascular smooth muscle cell culture showed spindle-like cells and obvious smooth muscle cell layer. Cell proteomics analysis showed that decreased expression of 118 proteins and increased expression of 32 proteins in smooth muscle cells after cyclic mechanical stretch. KEGG pathway analysis indicated that focal adhesion and ECM-receptor interaction were involved. After cyclic mechanical stretch, collagen type IV and IV expression were decreased. Moreover, the stretch induced MMP-1 and MMP-3 expression elevation. <b><i>Conclusion:</i></b> We demonstrated that collagen type IV and VI were decreased in cerebral aneurysms and continuous cyclic mechanical stretch induced smooth muscle cell changes. Smooth muscle cell protection provides an additional therapeutic option to prevent the growth of cerebral aneurysms.
DOI: 10.6084/m9.figshare.5882512.v1
title: Supplementary Material for: Cyclic Mechanical Stretch Induced Smooth Muscle Cell Changes in Cerebral Aneurysm Progress by Reducing Collagen Type IV and Collagen Type VI Levels

description: <b><i>Background/Aims:</i></b> Cerebral aneurysm growth is characterized by continuous structural weakness of local smooth muscle cells, though the mechanism is unclear. In this study, we examine protein changes in cerebral aneurysm and human brain vascular smooth muscle cells after cyclic mechanical stretch. We further explore the relationship between the smooth muscle cell changes and reductions in the levels of collagen types IV and VI. <b><i>Methods:</i></b> Saccular cerebral aneurysms (n=10) were collected, and temporal artery samples were used as controls. Quantitative proteomics were analyzed and histopathological changes were examined. Smooth muscle cells were cultured in a flexible silicone chamber and subjected to 15% cyclic mechanical stretch. The effect of stretch on the cell viability, function, gene and protein expression were further studied for the understanding the molecular mechanism of aneurysm development. <b><i>Results:</i></b> Proteomics analysis revealed 92 proteins with increased expression and 88 proteins with decreased expression compared to the controls (<i>p</i>&lt;0.05). KEGG pathway analysis showed that the change in focal adhesion and extracellular matrix-receptor interaction, suggesting the involvement of collagen type IV and VI. The aneurysm tissue exhibited fewer smooth muscle cells and lower levels of collagen type IV and VI. Human brain vascular smooth muscle cell culture showed spindle-like cells and obvious smooth muscle cell layer. Cell proteomics analysis showed that decreased expression of 118 proteins and increased expression of 32 proteins in smooth muscle cells after cyclic mechanical stretch. KEGG pathway analysis indicated that focal adhesion and ECM-receptor interaction were involved. After cyclic mechanical stretch, collagen type IV and IV expression were decreased. Moreover, the stretch induced MMP-1 and MMP-3 expression elevation. <b><i>Conclusion:</i></b> We demonstrated that collagen type IV and VI were decreased in cerebral aneurysms and continuous cyclic mechanical stretch induced smooth muscle cell changes. Smooth muscle cell protection provides an additional therapeutic option to prevent the growth of cerebral aneurysms.
DOI: 10.6084/m9.figshare.5882485
title: Supplementary Material for: Transgenic Overexpression of IL-37 Protects Against Atherosclerosis and Strengthens Plaque Stability

description: <b><i>Background/Aims:</i></b> Recently, studies have shown that interleukin-37 (IL-37) is involved in atherosclerosis-related diseases. However, the regulatory mechanisms of IL-37 in atherosclerosis remain unknown. This study aims to determine the role of IL-37 in atherosclerosis and to investigate the underlying mechanisms involved. <b><i>Methods:</i></b> IL-37 expression in human atherosclerotic plaques was detected by immunohistochemical staining and real-time reverse transcription polymerase chain reaction (RT-PCR). Oil Red O staining was used to measure the size of plaques. Cell apoptosis <i>in vitro</i> and <i>in vivo</i> was tested by flow cytometric analysis and terminal deoxynucleotidyl-transferase mediated dUTP nick-end labeling (TUNEL) staining, respectively. Protein expression levels of IL-37, IL-18Rα and p-Smad3 were measured by Weston blotting. <b><i>Results:</i></b> Immunohistochemical staining revealed that IL-37 was highly expressed in human atherosclerotic plaques. Intracellular cytokine staining revealed that infiltrated CD4<sup>+</sup> T lymphocytes and vascular smooth muscle cells (VSMCs), but not macrophages, were the major sources of IL-37. Mice that overexpressed IL-37 exhibited significant improvements in their atherosclerotic burden, as demonstrated by reduced plaque size, increased collagen levels, and reduced numbers of apoptotic cells <i>in vivo</i>. Subsequently, mechanistic studies showed that IL-37 played an anti-atherosclerotic role, at least partially, through reducing inflammation by promoting the differentiation of the T helper cell anti-inflammatory phenotype, and through increasing plaque stability by decreasing matrix metalloproteinase (MMP)-2/13-mediated degradation of collagen and inhibiting VSMCs apoptosis. <b><i>Conclusion:</i></b> IL-37 may be a novel potential therapeutic target in patients with atherosclerotic heart disease.
DOI: 10.6084/m9.figshare.5882485.v1
title: Supplementary Material for: Transgenic Overexpression of IL-37 Protects Against Atherosclerosis and Strengthens Plaque Stability

description: <b><i>Background/Aims:</i></b> Recently, studies have shown that interleukin-37 (IL-37) is involved in atherosclerosis-related diseases. However, the regulatory mechanisms of IL-37 in atherosclerosis remain unknown. This study aims to determine the role of IL-37 in atherosclerosis and to investigate the underlying mechanisms involved. <b><i>Methods:</i></b> IL-37 expression in human atherosclerotic plaques was detected by immunohistochemical staining and real-time reverse transcription polymerase chain reaction (RT-PCR). Oil Red O staining was used to measure the size of plaques. Cell apoptosis <i>in vitro</i> and <i>in vivo</i> was tested by flow cytometric analysis and terminal deoxynucleotidyl-transferase mediated dUTP nick-end labeling (TUNEL) staining, respectively. Protein expression levels of IL-37, IL-18Rα and p-Smad3 were measured by Weston blotting. <b><i>Results:</i></b> Immunohistochemical staining revealed that IL-37 was highly expressed in human atherosclerotic plaques. Intracellular cytokine staining revealed that infiltrated CD4<sup>+</sup> T lymphocytes and vascular smooth muscle cells (VSMCs), but not macrophages, were the major sources of IL-37. Mice that overexpressed IL-37 exhibited significant improvements in their atherosclerotic burden, as demonstrated by reduced plaque size, increased collagen levels, and reduced numbers of apoptotic cells <i>in vivo</i>. Subsequently, mechanistic studies showed that IL-37 played an anti-atherosclerotic role, at least partially, through reducing inflammation by promoting the differentiation of the T helper cell anti-inflammatory phenotype, and through increasing plaque stability by decreasing matrix metalloproteinase (MMP)-2/13-mediated degradation of collagen and inhibiting VSMCs apoptosis. <b><i>Conclusion:</i></b> IL-37 may be a novel potential therapeutic target in patients with atherosclerotic heart disease.
DOI: 10.6084/m9.figshare.5882482
title: Supplementary Material for: Hoxa5 Promotes Adipose Differentiation via Increasing DNA Methylation Level and Inhibiting PKA/HSL Signal Pathway in Mice

description: <b><i>Background/Aims:</i></b> Impaired adipogenesis may be the underlying cause in the development of obesity and type II diabetes. Mechanistically, the family of Homeobox transcription factors is implicated in the regulation of adipocyte fate. Hoxa5 is highly expressed in adipocytes, and its mRNA expression is decreased during differentiation. However, the function of Hoxa5 in adipose tissue has been poorly understood. The aim of this study is to unveil the role of Hoxa5 on adipocyte differentiation and its underlying mechanisms. <b><i>Methods:</i></b> Quantitative real-time PCR (qPCR) and western blot were performed to determine Hoxa5 expression in primary adipocytes and in adipose tissues from mice. Lipid accumulation was evaluated by bodipy staining. Dual luciferase assay was applied to explore the transcription factor of Hoxa5 and the transcriptional target gene modulated by Hoxa5. All measurements were performed at least for three times at least. <b><i>Results:</i></b> A significant reduction of Hoxa5 expression was observed in adipose tissue of High Fat Diet (HFD) induced obesity mice. We determined Hoxa5 increased adipocytes differentiation and mitochondrial biogenesis in adipocytes <i>in vitro</i>. CEBPβ was determined a transcription factor of Hoxa5 and inhibited methylation level of Hoxa5 by combining on the promoter of Hoxa5. Importantly, we found Fabp4, a known positive regulator of adipocytes differentiation, was transcriptional activation by Hoxa5. In addition, Hoxa5 promotes adipocytes differentiation by inhibiting PKA/HSL pathway. <b><i>Conclusion:</i></b> Our study demonstrated the promoting role of Hoxa5 in adipocytes differentiation and therefore bringing a new therapeutic mean to the treatment of obesity and type II diabetes.
DOI: 10.6084/m9.figshare.5882479
title: All pregabalin data 2010-08 to 2017-10

description: An extract of all prescribing of pregabalin capsules per practice and month obtained via BigQuery from NHS Digital prescribing data set
DOI: 10.6084/m9.figshare.5882482.v1
title: Supplementary Material for: Hoxa5 Promotes Adipose Differentiation via Increasing DNA Methylation Level and Inhibiting PKA/HSL Signal Pathway in Mice

description: <b><i>Background/Aims:</i></b> Impaired adipogenesis may be the underlying cause in the development of obesity and type II diabetes. Mechanistically, the family of Homeobox transcription factors is implicated in the regulation of adipocyte fate. Hoxa5 is highly expressed in adipocytes, and its mRNA expression is decreased during differentiation. However, the function of Hoxa5 in adipose tissue has been poorly understood. The aim of this study is to unveil the role of Hoxa5 on adipocyte differentiation and its underlying mechanisms. <b><i>Methods:</i></b> Quantitative real-time PCR (qPCR) and western blot were performed to determine Hoxa5 expression in primary adipocytes and in adipose tissues from mice. Lipid accumulation was evaluated by bodipy staining. Dual luciferase assay was applied to explore the transcription factor of Hoxa5 and the transcriptional target gene modulated by Hoxa5. All measurements were performed at least for three times at least. <b><i>Results:</i></b> A significant reduction of Hoxa5 expression was observed in adipose tissue of High Fat Diet (HFD) induced obesity mice. We determined Hoxa5 increased adipocytes differentiation and mitochondrial biogenesis in adipocytes <i>in vitro</i>. CEBPβ was determined a transcription factor of Hoxa5 and inhibited methylation level of Hoxa5 by combining on the promoter of Hoxa5. Importantly, we found Fabp4, a known positive regulator of adipocytes differentiation, was transcriptional activation by Hoxa5. In addition, Hoxa5 promotes adipocytes differentiation by inhibiting PKA/HSL pathway. <b><i>Conclusion:</i></b> Our study demonstrated the promoting role of Hoxa5 in adipocytes differentiation and therefore bringing a new therapeutic mean to the treatment of obesity and type II diabetes.
DOI: 10.6084/m9.figshare.5882479.v1
title: All pregabalin data 2010-08 to 2017-10

description: An extract of all prescribing of pregabalin capsules per practice and month obtained via BigQuery from NHS Digital prescribing data set
DOI: 10.6084/m9.figshare.5882470
title: Pregabalin prescribing data - March to August 2015

description: An extract of all prescribing of pregabalin capsules per practice and month obtained via BigQuery from NHS Digital prescribing data set