cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5255/ukda-sn-856533
title: Digital Sovereignty by Design, Academic Articles and Policy Papers, 2023

description: Datasets present text data stemming from academic articles (Scopus and WoS) and Policy documents collected from EU institutional repositories (European Commission, European Parliament, Council of the European Union). The data was collected from January to May 2023, as part of the "Digital Sovereignty by Design" research project framework. The primary purpose of this data collection is to conduct topic modelling, namely Latent Dirichlet Allocation (LDA), in order to identify current debates on digital sovereignty through international relations and political science lenses. 

We seek to identify and demonstrate the state-of-the-art with revealing trends and insights, mapping complex research and the political landscape of digital sovereignty issues in the EU. The objectives are (1) to identify the role played by the concept of digital sovereignty in different fields of studies; (2) to highlight recent trends in the study of digital sovereignty; (3) to identify, within those trends, the most common topics related to digital sovereignty and to trace their development over time; and (4) to explore how those trends and topics related to political regulation and governance within the digital sovereignty sphere.

We present five datasets. One dataset contained academic articles data on digital sovereignty, and four other datasets collected policy documents from EU institutions.
The academic articles' datasets contain complete bibliographic information, abstract and keywords (if available) from 2013 to 2023 with a total N of 156 texts. The datasets for the policy documents include the document's title and its complete text: European Commission from 2009 to 2023 with a total N of 2019 texts (61 from Register; 158 from Commonly used documents); European Parliament from 2011 to 2023 with total N of 368 texts; and Council of the European Union from 2001 to 2023 with total N of 221 texts.
DOI: 10.6084/m9.figshare.24949280
title: Association between mutations in a <i>thyX-hsdS.1</i> region and <i>para</i>-aminosalicylic acid resistance in <i>Mycobacterium tuberculosis</i> clinical isolates

description: Although <i>para</i>-aminosalicylic acid (PAS) has been used to treat tuberculosis agent for decades, its mechanisms of resistance are still not thoroughly understood. Previously, sporadic studies showed that certain mutations in the <i>thyX-hsdS.1</i> region caused PAS resistance in <i>M. tuberculosis</i>, but a comprehensive analysis is lacking. Recently, we found a G–10A mutation in <i>thyX-hsdS.1</i> in a PAS-resistant clinical isolate, but it did not cause PAS resistance. SNPs in <i>thyX-hsdS.1</i> in 6550 clinical isolates were analyzed, and 153 SNPs were identified. C–16 T was the most common SNP identified (54.25%, 83/153), followed by C–4T (7.19%, 11/153) and G–9A (6.54%, 10/153). Subsequently, the effects of those SNPs on the promoter activity of <i>thyX</i> were tested, and the results showed that mutations C–1T, G–3A, C–4T, C–4G, G–7A, G–9A, C–16T, G–18C, and C–19G led to increased promoter activity compared with the wild-type sequence, but other mutations did not. Then, <i>thyX</i> and wild-type <i>thyX-hsdS.1</i>, or <i>thyX-hsdS.1</i> containing specific SNPs, were overexpressed in <i>M. tuberculosis</i> H37Ra. The results showed that mutations resulting in increased promoter activity also caused PAS resistance. Moreover, the results of an electrophoretic mobility shift assay showed that <i>thyX-hsdS.1</i> containing the C–16T mutation had a higher binding capacity to RNA polymerase than did the wild-type sequence. Taken together, our data demonstrated that among the SNPs identified in <i>thyX-hsdS.1</i> of <i>M. tuberculosis</i> clinical isolates, only those able to increase the promoter activity of <i>thyX</i> caused PAS resistance and therefore can be considered as molecular markers for PAS resistance.
DOI: 10.6084/m9.figshare.24949280.v1
title: Association between mutations in a <i>thyX-hsdS.1</i> region and <i>para</i>-aminosalicylic acid resistance in <i>Mycobacterium tuberculosis</i> clinical isolates

description: Although <i>para</i>-aminosalicylic acid (PAS) has been used to treat tuberculosis agent for decades, its mechanisms of resistance are still not thoroughly understood. Previously, sporadic studies showed that certain mutations in the <i>thyX-hsdS.1</i> region caused PAS resistance in <i>M. tuberculosis</i>, but a comprehensive analysis is lacking. Recently, we found a G–10A mutation in <i>thyX-hsdS.1</i> in a PAS-resistant clinical isolate, but it did not cause PAS resistance. SNPs in <i>thyX-hsdS.1</i> in 6550 clinical isolates were analyzed, and 153 SNPs were identified. C–16 T was the most common SNP identified (54.25%, 83/153), followed by C–4T (7.19%, 11/153) and G–9A (6.54%, 10/153). Subsequently, the effects of those SNPs on the promoter activity of <i>thyX</i> were tested, and the results showed that mutations C–1T, G–3A, C–4T, C–4G, G–7A, G–9A, C–16T, G–18C, and C–19G led to increased promoter activity compared with the wild-type sequence, but other mutations did not. Then, <i>thyX</i> and wild-type <i>thyX-hsdS.1</i>, or <i>thyX-hsdS.1</i> containing specific SNPs, were overexpressed in <i>M. tuberculosis</i> H37Ra. The results showed that mutations resulting in increased promoter activity also caused PAS resistance. Moreover, the results of an electrophoretic mobility shift assay showed that <i>thyX-hsdS.1</i> containing the C–16T mutation had a higher binding capacity to RNA polymerase than did the wild-type sequence. Taken together, our data demonstrated that among the SNPs identified in <i>thyX-hsdS.1</i> of <i>M. tuberculosis</i> clinical isolates, only those able to increase the promoter activity of <i>thyX</i> caused PAS resistance and therefore can be considered as molecular markers for PAS resistance.
DOI: 10.6084/m9.figshare.24949283
title: Analysis of the interplay between MeCP2 and histone H1 during <i>in vitro</i> differentiation of human ReNCell neural progenitor cells

description: An immortalized neural cell line derived from the human ventral mesencephalon, called ReNCell, and its MeCP2 knock out were used. With it, we characterized the chromatin compositional transitions undergone during differentiation, with special emphasis on linker histones. While the WT cells displayed the development of dendrites and axons the KO cells did not, despite undergoing differentiation as monitored by NeuN. ReNCell expressed minimal amounts of histone H1.0 and their linker histone complement consisted mainly of histone H1.2, H1.4 and H1.5. The overall level of histone H1 exhibited a trend to increase during the differentiation of MeCP2 KO cells. The phosphorylation levels of histone H1 proteins decreased dramatically during ReNCell’s cell differentiation independently of the presence of MeCP2. Immunofluorescence analysis showed that MeCP2 exhibits an extensive co-localization with linker histones. Interestingly, the average size of the nucleus decreased during differentiation but in the MeCP2 KO cells, the smaller size of the nuclei at the start of differentiation increased by almost 40% after differentiation by 8 days (8 DIV). In summary, our data provide a compelling perspective on the dynamic changes of H1 histones during neural differentiation, coupled with the intricate interplay between H1 variants and MeCP2. <b>Abbreviations</b>: ACN, acetonitrile; A<sub>230</sub>, absorbance at 230 nm; bFGF, basic fibroblast growth factor; CM, chicken erythrocyte histone marker; CNS, central nervous system; CRISPR, clustered regulated interspaced short palindromic repeatsDAPI, 4,’6-diaminidino-2-phenylindole; DIV, days <i>in vitro</i> (days after differentiation is induced); DMEM, Dulbecco’s modified Eagle medium; EGF, epidermal growth factor; ESC, embryonic stem cell; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GFAP, glial fibrillary acidic proteinHPLC, high-performance liquid chromatography; IF, immunofluorescence; iPSCs, induced pluripotent stem cells; MAP2, microtubule-associated protein 2; MBD, methyl-binding domain; MeCP2, methyl-CpG binding protein 2; MS, mass spectrometry; NCP, nucleosome core particle; NeuN, neuron nuclear antigen; NPC, neural progenitor cellPAGE, polyacrylamide gel electrophoresis; PBS, phosphate buffered saline; PFA, paraformaldehyde; PTM, posttranslational modification; RP-HPLC, reversed phase HPLC; ReNCells, ReNCells VM; RPLP0, ribosomal protein lateral stalk subunit P0; RT-qPCR, reverse transcription quantitative polymerase-chain reaction; RTT, Rett Syndrome; SDS, sodium dodecyl sulphate; TAD, topologically associating domain; Triple KO, triple knockout.
DOI: 10.6084/m9.figshare.24949283.v1
title: Analysis of the interplay between MeCP2 and histone H1 during <i>in vitro</i> differentiation of human ReNCell neural progenitor cells

description: An immortalized neural cell line derived from the human ventral mesencephalon, called ReNCell, and its MeCP2 knock out were used. With it, we characterized the chromatin compositional transitions undergone during differentiation, with special emphasis on linker histones. While the WT cells displayed the development of dendrites and axons the KO cells did not, despite undergoing differentiation as monitored by NeuN. ReNCell expressed minimal amounts of histone H1.0 and their linker histone complement consisted mainly of histone H1.2, H1.4 and H1.5. The overall level of histone H1 exhibited a trend to increase during the differentiation of MeCP2 KO cells. The phosphorylation levels of histone H1 proteins decreased dramatically during ReNCell’s cell differentiation independently of the presence of MeCP2. Immunofluorescence analysis showed that MeCP2 exhibits an extensive co-localization with linker histones. Interestingly, the average size of the nucleus decreased during differentiation but in the MeCP2 KO cells, the smaller size of the nuclei at the start of differentiation increased by almost 40% after differentiation by 8 days (8 DIV). In summary, our data provide a compelling perspective on the dynamic changes of H1 histones during neural differentiation, coupled with the intricate interplay between H1 variants and MeCP2. <b>Abbreviations</b>: ACN, acetonitrile; A<sub>230</sub>, absorbance at 230 nm; bFGF, basic fibroblast growth factor; CM, chicken erythrocyte histone marker; CNS, central nervous system; CRISPR, clustered regulated interspaced short palindromic repeatsDAPI, 4,’6-diaminidino-2-phenylindole; DIV, days <i>in vitro</i> (days after differentiation is induced); DMEM, Dulbecco’s modified Eagle medium; EGF, epidermal growth factor; ESC, embryonic stem cell; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GFAP, glial fibrillary acidic proteinHPLC, high-performance liquid chromatography; IF, immunofluorescence; iPSCs, induced pluripotent stem cells; MAP2, microtubule-associated protein 2; MBD, methyl-binding domain; MeCP2, methyl-CpG binding protein 2; MS, mass spectrometry; NCP, nucleosome core particle; NeuN, neuron nuclear antigen; NPC, neural progenitor cellPAGE, polyacrylamide gel electrophoresis; PBS, phosphate buffered saline; PFA, paraformaldehyde; PTM, posttranslational modification; RP-HPLC, reversed phase HPLC; ReNCells, ReNCells VM; RPLP0, ribosomal protein lateral stalk subunit P0; RT-qPCR, reverse transcription quantitative polymerase-chain reaction; RTT, Rett Syndrome; SDS, sodium dodecyl sulphate; TAD, topologically associating domain; Triple KO, triple knockout.
DOI: 10.6084/m9.figshare.20226812.v1
title: Additional file 11 of Combined nature and human selections reshaped peach fruit metabolome

description: Additional file 11: Table S10. Number of associated SNPs in each non-overlapping 1-Mb sliding windows across the peach genome.
DOI: 10.6084/m9.figshare.19178990.v1
title: Additional file 2 of Development of an efficient and precise adenine base editor (ABE) with expanded target range in allotetraploid cotton (Gossypium hirsutum)

description: Additional file 2: Supplementary tables 1-7. Table S1. Primers used for vectors construction. Table S2. Primers used for positive test. Table S3. Barcode primers for detecting off-target in base editing T0 transgenic plants with deep sequencing for GhPEBE gene. Table S4. Barcode primers for detecting off-target in base editing T0 transgenic plants with deep sequencing for GhCLA gene. Table S5. Summary of genome-wide potential off-targets predictions by Cas-OFFinder tools for target sgRNA1. Table S6. Summary of genome-wide potential off-targets predictions by Cas-OFFinder tools for target sgRNA2. Table S7. Expression levels (TPM) of TadA, nCas9 and dCas9 in GhABE7.10 edited plant.
DOI: 10.6084/m9.figshare.14985057.v1
title: Additional file 7 of Somatic mutations in benign breast disease tissues and association with breast cancer risk

description: Additional file 7. Table S3: Gene-level results for case-control comparisons for all 12 combinations of QC filters and analysis methods.
DOI: 10.6084/m9.figshare.14985060
title: Additional file 8 of Somatic mutations in benign breast disease tissues and association with breast cancer risk

description: Additional file 8. Table S4: Gene-level results for ER+ vs. Control comparisons for all 12 combinations of QC filters and analysis methods.
DOI: 10.6084/m9.figshare.14985054
title: Additional file 6 of Somatic mutations in benign breast disease tissues and association with breast cancer risk

description: Additional file 6. Table S2: Estimates for the de-novo signatures A-D and previously estimated QGR and FFPE signatures by mutation category.
DOI: 10.6084/m9.figshare.14463711
title: Output files(part3)

description: The output files of MIP3D.
DOI: 10.6084/m9.figshare.14463711.v1
title: Output files(part3)

description: The output files of MIP3D.
DOI: 10.6084/m9.figshare.14463714
title: Output files(part4)

description: The output files of MIP3D.
DOI: 10.6084/m9.figshare.14463714.v1
title: Output files(part4)

description: The output files of MIP3D.
DOI: 10.6084/m9.figshare.14463717
title: Output files(part5)

description: The output files of MIP3D.
DOI: 10.6084/m9.figshare.14463717.v1
title: Output files(part5)

description: The output files of MIP3D.
DOI: 10.6084/m9.figshare.14463720
title: Output files(part6)

description: The output files of MIP3D.
DOI: 10.6084/m9.figshare.14463720.v1
title: Output files(part6)

description: The output files of MIP3D.
DOI: 10.6084/m9.figshare.8172341
title: Additional file 5: of The prominent alteration in transcriptome and metabolome of Mycobacterium bovis BCG str. Tokyo 172 induced by vitamin B1

description: Table S5. The complete list of detected amino acids in control and VB1-treated samples. (XLSX 23 kb)
DOI: 10.6084/m9.figshare.14988096.v1
title: Data_File_2.csv

description: Values underlying Fig. 4b for ECO-BB sensor
DOI: 10.6084/m9.figshare.8172365.v1
title: Additional file 4: of Genomic evidence of the illumination response mechanism and evolutionary history of magnetotactic bacteria within the Rhodospirillaceae family

description: Table S3 A. The core inventory shared by the family Rhodospirillaceae; Table S3 B. The core genes among MTB, phototrophic bacteria, non-phototrophic non-magnetotactic bacteria within Rhodospirillaceae and other MTB that are not related to the family Rhodospirillaceae (XLSX 178 kb)
DOI: 10.6084/m9.figshare.8172428
title: MOESM1 of Development of large-scale mosquito densovirus production by in vivo methods

description: Additional file 1: Table S1. Primers and amplification conditions for PCR and qPCR assays.
DOI: 10.6084/m9.figshare.19703487
title: Ganoderic Acid A alleviates the degeneration of intervertebral disc via suppressing the activation of TLR4/NLRP3 signaling pathway

description: As a multifactorial disease, intervertebral disc degeneration (IVDD) causes many spinal-related diseases, which causes disability in the workforce and heavy social costs all over the world. Recently, Ganoderic Acid A (GAA) has been reported to play many pharmacological effects. However, its effect on IVDD remains unclear. In the present study, our study determined that GAA significantly inhibited H<sub>2</sub>O<sub>2</sub> induced apoptosis, release of inflammatory cytokines and oxidative stress mediators in the nucleus pulposus (NP) cells. Moreover, GAA also suppressed H<sub>2</sub>O<sub>2</sub> induced major matrix degrading proteases (MMP-3, MMP-13, ADAMTS4 and ADAMTS5) associated with NP degradation. Additionally, we found NP protective ability of GAA by up-regulating extra cellular matrix anabolic factors like type II collagen (Col II) and aggrecan in NP cells. Furthermore, we also demonstrated that GAA suppressed the activation of TLR4/NLRP3 in H<sub>2</sub>O<sub>2</sub>-stimulated NP cells. Thus, our results demonstrate that GAA inhibited the H<sub>2</sub>O<sub>2</sub> induced apoptosis, oxidative stress, and inflammatory responses through the depression of TLR4/NLRP3 signaling axis. GAA possess NP protective properties and may be of value in suppressing the pathogenesis of IVDD.
DOI: 10.6084/m9.figshare.14985045.v1
title: Additional file 3 of Somatic mutations in benign breast disease tissues and association with breast cancer risk

description: Additional file 3. Table S1: Meta-data table for all study samples and quality control samples including total number of variants, mean coverage, genotype call rate, and clinical covariates.
DOI: 10.6084/m9.figshare.14985054.v1
title: Additional file 6 of Somatic mutations in benign breast disease tissues and association with breast cancer risk

description: Additional file 6. Table S2: Estimates for the de-novo signatures A-D and previously estimated QGR and FFPE signatures by mutation category.
DOI: 10.6084/m9.figshare.14985060.v1
title: Additional file 8 of Somatic mutations in benign breast disease tissues and association with breast cancer risk

description: Additional file 8. Table S4: Gene-level results for ER+ vs. Control comparisons for all 12 combinations of QC filters and analysis methods.
DOI: 10.6084/m9.figshare.20226818.v1
title: Additional file 13 of Combined nature and human selections reshaped peach fruit metabolome

description: Additional file 13: Table S12. Differentially expressed genes detected during domestication (sheet 1), improvement (sheet 2), and differentiation (sheet 3).
DOI: 10.6084/m9.figshare.14984852.v1
title: Additional file 7 of Differential gene expression patterns during gametophyte development provide insights into sex differentiation in the dioicous kelp Saccharina japonica

description: Additional file 7: Table S7. Sex-specific genes of S. japonica at the different stages.
DOI: 10.6084/m9.figshare.7645061
title: Electronic supplementary material from Study on ground settlement and structural deformation for large span subway station using a new pre-supporting system

description: Data used in the manuscript
DOI: 10.6084/m9.figshare.14984846
title: Additional file 5 of Differential gene expression patterns during gametophyte development provide insights into sex differentiation in the dioicous kelp Saccharina japonica

description: Additional file 5: Table S5. Enriched GO terms of female-biased genes in both immature and mature gametophytes.
DOI: 10.6084/m9.figshare.14984855
title: Additional file 8 of Differential gene expression patterns during gametophyte development provide insights into sex differentiation in the dioicous kelp Saccharina japonica

description: Additional file 8: Table S8. Information on gametophytes used in this study.
DOI: 10.6084/m9.figshare.14984846.v1
title: Additional file 5 of Differential gene expression patterns during gametophyte development provide insights into sex differentiation in the dioicous kelp Saccharina japonica

description: Additional file 5: Table S5. Enriched GO terms of female-biased genes in both immature and mature gametophytes.
DOI: 10.6084/m9.figshare.14984855.v1
title: Additional file 8 of Differential gene expression patterns during gametophyte development provide insights into sex differentiation in the dioicous kelp Saccharina japonica

description: Additional file 8: Table S8. Information on gametophytes used in this study.
DOI: 10.6084/m9.figshare.19703531
title: lncRNA H19 promotes glioblastoma multiforme development by activating autophagy by sponging miR-491-5p

description: Glioblastoma multiforme (GBM) is a malignant cancer with severely poor survival, and the cells continue to thrive during hypoxia and toxic stress through autophagy. To validate the oncogenic role of long noncoding RNA H19 in GBM progression and examine whether autophagy and/or miR-491-5p participate in the process. The expression of H19 and autophagy-related genes in GBM and healthy control tissues was assessed via quantitative polymerase chain reaction. In addition, cell viability, proliferation, apoptosis and autophagy were respectively determined via cell counting kit-8 assay, clone formation assay, flow cytometry, western blotting and green fluorescent protein–microtubule-associated protein 1 light chain 3 alpha fluorescence analysis <i>in vitro</i>. Furthermore, a rescue assay was performed using rapamycin or miR-491-5p antagomir to examine the role of autophagy or miR-491-5p in H19-mediated regulation of proliferation and apoptosis. RNA pull-down and dual-luciferase reporter assays were employed to analyze the interaction between H19 and miR-491-5p. Additionally, tumor growth in a xenograft-bearing mouse model and autophagy in tumor mass were analyzed <i>in vivo</i>. The expression H19 was increased in GBM and was positively correlated with LC3 or Beclin-1. Silencing H19 inhibited growth and promoted apoptosis in GBM cells both <i>in vitro</i> and <i>in vivo</i>, and miR-491-5p was identified as one of the important mediators. H19 regulated the autophagy signaling pathway at least partly via miR-491-5p. Increased H19 expression in GBM exerts oncogenic effects by sponging miR-491-5p and enhancing autophagy. Therefore, H19 may be explored as a target for GBM therapy.
DOI: 10.6084/m9.figshare.19703531.v1
title: lncRNA H19 promotes glioblastoma multiforme development by activating autophagy by sponging miR-491-5p

description: Glioblastoma multiforme (GBM) is a malignant cancer with severely poor survival, and the cells continue to thrive during hypoxia and toxic stress through autophagy. To validate the oncogenic role of long noncoding RNA H19 in GBM progression and examine whether autophagy and/or miR-491-5p participate in the process. The expression of H19 and autophagy-related genes in GBM and healthy control tissues was assessed via quantitative polymerase chain reaction. In addition, cell viability, proliferation, apoptosis and autophagy were respectively determined via cell counting kit-8 assay, clone formation assay, flow cytometry, western blotting and green fluorescent protein–microtubule-associated protein 1 light chain 3 alpha fluorescence analysis <i>in vitro</i>. Furthermore, a rescue assay was performed using rapamycin or miR-491-5p antagomir to examine the role of autophagy or miR-491-5p in H19-mediated regulation of proliferation and apoptosis. RNA pull-down and dual-luciferase reporter assays were employed to analyze the interaction between H19 and miR-491-5p. Additionally, tumor growth in a xenograft-bearing mouse model and autophagy in tumor mass were analyzed <i>in vivo</i>. The expression H19 was increased in GBM and was positively correlated with LC3 or Beclin-1. Silencing H19 inhibited growth and promoted apoptosis in GBM cells both <i>in vitro</i> and <i>in vivo</i>, and miR-491-5p was identified as one of the important mediators. H19 regulated the autophagy signaling pathway at least partly via miR-491-5p. Increased H19 expression in GBM exerts oncogenic effects by sponging miR-491-5p and enhancing autophagy. Therefore, H19 may be explored as a target for GBM therapy.