cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.806022
title: Eeg Motor Imagery Dataset From The Phd Thesis "Commande Robuste D'Un Effecteur Par Une Interface Cerveau Machine Eeg Asynchrone"

description: This Dataset contains EEG recordings from 8 subjects, performing 2 task of motor imagination (right hand, feet or rest). Data have been recorded at 512Hz with 16 wet electrodes (Fpz, F7, F3, Fz, F4, F8, T7, C3, Cz, C4, T8, P7, P3, Pz, P4, P8) with a g.tec g.USBamp EEG amplifier.

File are provided in MNE raw file format. A stimulation channel encoding the timing of the motor imagination. The start of a trial is encoded as 1, then the actual start of the motor imagination is encoded with 2 for imagination of a right hand movement, 3 for imagination of both feet movement and 4 with a rest trial.

The duration of each trial is 3 second. There is 20 trial of each class.
DOI: 10.5281/zenodo.806023
title: Eeg Motor Imagery Dataset From The Phd Thesis "Commande Robuste D'Un Effecteur Par Une Interface Cerveau Machine Eeg Asynchrone"

description: This Dataset contains EEG recordings from 8 subjects, performing 2 task of motor imagination (right hand, feet or rest). Data have been recorded at 512Hz with 16 wet electrodes (Fpz, F7, F3, Fz, F4, F8, T7, C3, Cz, C4, T8, P7, P3, Pz, P4, P8) with a g.tec g.USBamp EEG amplifier.

File are provided in MNE raw file format. A stimulation channel encoding the timing of the motor imagination. The start of a trial is encoded as 1, then the actual start of the motor imagination is encoded with 2 for imagination of a right hand movement, 3 for imagination of both feet movement and 4 with a rest trial.

The duration of each trial is 3 second. There is 20 trial of each class.
DOI: 10.5517/ccdc.csd.cc1nvkz1
title: CCDC 1544884: Experimental Crystal Structure Determination

description: Related Article: Maria A. Susano, Pablo Martín-Ramos, Teresa M.R. Maria, Steven Folkersma, Laura C.J. Pereira, Manuela Ramos Silva|2017|J.Mol.Struct.|1147|76|doi:10.1016/j.molstruc.2017.06.043
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc1nvrbl
title: CCDC 1545050: Experimental Crystal Structure Determination

description: Related Article: Gorkem Oylumluoglu, Mustafa Burak Coban, Cagdas Kocak, Muhittin Aygun, Hulya Kara|2017|J.Mol.Struct.|1146|356|doi:10.1016/j.molstruc.2017.06.020
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc1nvrcm
title: CCDC 1545051: Experimental Crystal Structure Determination

description: Related Article: Gorkem Oylumluoglu, Mustafa Burak Coban, Cagdas Kocak, Muhittin Aygun, Hulya Kara|2017|J.Mol.Struct.|1146|356|doi:10.1016/j.molstruc.2017.06.020
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc1nwqt2
title: CCDC 1545995: Experimental Crystal Structure Determination

description: Related Article: Sakkani Nagaraju, Kota Sathish, Banoth Paplal, Dhurke Kashinath|2017|Tetrahedron Lett.|58|2865|doi:10.1016/j.tetlet.2017.06.029
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5281/zenodo.804007
title: Formatting Hemiclone Drosophila Melanogaster Genotype Data For Gwas

description: Data and code for generating filtering and formatting of Drosophila melanogaster genotype data, from the Sussex LHM hemiclone population sample.
description: {"references": ["doi: 10.12688/f1000research.9912.3"]}
DOI: 10.5281/zenodo.804008
title: Formatting Hemiclone Drosophila Melanogaster Genotype Data For Gwas

description: Data and code for generating filtering and formatting of Drosophila melanogaster genotype data, from the Sussex LHM hemiclone population sample.
description: {"references": ["doi: 10.12688/f1000research.9912.3"]}
DOI: 10.17632/jsmbyfmck2.1
title: Data for: Excitation energy dependence of Raman spectra of few-layer WS2

description: Electronic Supplementary Information
DOI: 10.6084/m9.figshare.13266243.v1
title: Additional file 1 of Targeted mutagenesis of ∆5 and ∆6 fatty acyl desaturases induce dysregulation of lipid metabolism in Atlantic salmon (Salmo salar)

description: (XLSX 608 kb)
DOI: 10.6084/m9.figshare.20088015.v1
title: Additional file 5 of HBV genome-enriched single cell sequencing revealed heterogeneity in HBV-driven hepatocellular carcinoma (HCC)

description: Additional file 5: Table S4. Match with Poisson distribution. Reads distribution on human genome is tested against Poisson distribution. The null hypothesis is the reads mapped to human genome following Poisson distribution. The test consistently fails until the corresponding region covering 88% of human genome.
DOI: 10.6084/m9.figshare.20088030
title: Additional file 9 of HBV genome-enriched single cell sequencing revealed heterogeneity in HBV-driven hepatocellular carcinoma (HCC)

description: Additional file 9: Table S8. HBV integrations detected with WGS from MHCC97H. At least one soft clipped read and two adjacent reads are required to call HBV integration.
DOI: 10.25402/fon.20088260.v1
title: Supplementary Tables – Tumor Calcification is Associated with Better Survival in Metastatic Colorectal Cancer Patients Treated with Bevacizumab Plus Chemotherapy

description:       
<strong>Supplementary   table 1</strong>. Tumor Calcification is   Associated with Better Survival in Metastatic Colorectal Cancer Patients   Treated with Bevacizumab Plus Chemotherapy
<em>The doses of   bevacizumab and chemotherapy.</em>
<strong>Supplementary   table 2</strong>. Tumor Calcification is   Associated with Better Survival in Metastatic Colorectal Cancer Patients   Treated with Bevacizumab Plus Chemotherapy
<em>Response to   treatment in patients with calcification</em>
DOI: 10.6084/m9.figshare.13266249
title: Additional file 3 of Targeted mutagenesis of ∆5 and ∆6 fatty acyl desaturases induce dysregulation of lipid metabolism in Atlantic salmon (Salmo salar)

description: (CSV 3 kb)
DOI: 10.6084/m9.figshare.13266246
title: Additional file 2 of Targeted mutagenesis of ∆5 and ∆6 fatty acyl desaturases induce dysregulation of lipid metabolism in Atlantic salmon (Salmo salar)

description: (CSV 61 kb)
DOI: 10.6084/m9.figshare.20088009
title: Additional file 3 of HBV genome-enriched single cell sequencing revealed heterogeneity in HBV-driven hepatocellular carcinoma (HCC)

description: Additional file 3: Table S2. Reads distribution for HGE-scSeq from tumor, bulk tissue data from adjacent normal and HGE-scSeq from MHCC97H cells including number of raw reads, number of reads after filtering, number of reads pair-ended mapped to human genome, number of reads pair-ended mapped to HBV genome and number of soft clipped reads covering HBV integration site.
DOI: 10.6084/m9.figshare.20088090
title: Additional file 1 of Intratumoral fibrosis and patterns of immune infiltration in clear cell renal cell carcinoma

description: Additional file 1. The protein expression of tumor and adjacent normal tissues.
DOI: 10.6084/m9.figshare.20088093.v1
title: Additional file 2 of Intratumoral fibrosis and patterns of immune infiltration in clear cell renal cell carcinoma

description: Additional file 2. The protein expression of high fibrosis (HF) group and low fibrosis (LF) group tissues.
DOI: 10.6084/m9.figshare.20088090.v1
title: Additional file 1 of Intratumoral fibrosis and patterns of immune infiltration in clear cell renal cell carcinoma

description: Additional file 1. The protein expression of tumor and adjacent normal tissues.
DOI: 10.6084/m9.figshare.20088093
title: Additional file 2 of Intratumoral fibrosis and patterns of immune infiltration in clear cell renal cell carcinoma

description: Additional file 2. The protein expression of high fibrosis (HF) group and low fibrosis (LF) group tissues.
DOI: 10.6084/m9.figshare.20088141
title: Additional file 10 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 10. IP-MS data in this study.
DOI: 10.6084/m9.figshare.20088144.v1
title: Additional file 11 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 11. RNA-seq data in this study.
DOI: 10.6084/m9.figshare.20088141.v1
title: Additional file 10 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 10. IP-MS data in this study.
DOI: 10.6084/m9.figshare.20088180.v1
title: Additional file 8 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 8. shRNA target sequences used in this study.
DOI: 10.6084/m9.figshare.20088144
title: Additional file 11 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 11. RNA-seq data in this study.
DOI: 10.6084/m9.figshare.20088150
title: Additional file 13 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 13. Antibody used in this study.
DOI: 10.6084/m9.figshare.20088150.v1
title: Additional file 13 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 13. Antibody used in this study.
DOI: 10.6084/m9.figshare.20088180
title: Additional file 8 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 8. shRNA target sequences used in this study.
DOI: 10.6084/m9.figshare.20088183.v1
title: Additional file 9 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 9. RT-qPCR primers used in this study.
DOI: 10.6084/m9.figshare.20088147
title: Additional file 12 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 12. ATAC-seq TSS binding sites data in this study.
DOI: 10.25402/fon.20088260
title: Supplementary Tables – Tumor Calcification is Associated with Better Survival in Metastatic Colorectal Cancer Patients Treated with Bevacizumab Plus Chemotherapy

description:       
<strong>Supplementary   table 1</strong>. Tumor Calcification is   Associated with Better Survival in Metastatic Colorectal Cancer Patients   Treated with Bevacizumab Plus Chemotherapy
<em>The doses of   bevacizumab and chemotherapy.</em>
<strong>Supplementary   table 2</strong>. Tumor Calcification is   Associated with Better Survival in Metastatic Colorectal Cancer Patients   Treated with Bevacizumab Plus Chemotherapy
<em>Response to   treatment in patients with calcification</em>
DOI: 10.6084/m9.figshare.20088183
title: Additional file 9 of H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition

description: Additional file 9. RT-qPCR primers used in this study.
DOI: 10.6084/m9.figshare.20088203.v1
title: Additional file 7 of Gut dysbiosis promotes prostate cancer progression and docetaxel resistance via activating NF-κB-IL6-STAT3 axis

description: Additional file 7. Mouse (phylum to species).
DOI: 10.6084/m9.figshare.20088203
title: Additional file 7 of Gut dysbiosis promotes prostate cancer progression and docetaxel resistance via activating NF-κB-IL6-STAT3 axis

description: Additional file 7. Mouse (phylum to species).
DOI: 10.6084/m9.figshare.20088200.v1
title: Additional file 6 of Gut dysbiosis promotes prostate cancer progression and docetaxel resistance via activating NF-κB-IL6-STAT3 axis

description: Additional file 6. Human (phylum to species).
DOI: 10.6084/m9.figshare.20088200
title: Additional file 6 of Gut dysbiosis promotes prostate cancer progression and docetaxel resistance via activating NF-κB-IL6-STAT3 axis

description: Additional file 6. Human (phylum to species).
DOI: 10.6084/m9.figshare.21137119
title: Additional file 8 of Quality control recommendations for RNASeq using FFPE samples based on pre-sequencing lab metrics and post-sequencing bioinformatics metrics

description: Additional file 8. All sample related metrics including pre-sequencing lab metrics and post sequencing bioinformatics metrics.
DOI: 10.6084/m9.figshare.20088600.v1
title: Evaluation of the factors affecting lung function in pediatric patients with asthma

description: This study aimed to analyze the risk factors affecting lung function in children with asthma based on clinical data to advice on clinical treatment and prognosis. This study included newly diagnosed patients with asthma admitted to the Respiratory Department of Chengdu Women’s and Children’s Central Hospital in Sichuan from July 2020 to June 2021. The factors associated with lung function were analyzed using univariate and multivariate linear regression with the forward method, while factors affecting lung ventilation function were analyzed using multivariate logistic regression. Sixty percent of the patients had normal lung function. Age was significantly negatively correlated with forced vital capacity (FVC)/FVC<sub>predicted</sub> (<i>B</i> = –1.385, <i>p</i> = 0.001), FEV<sub>1</sub>/FEV<sub>1predicted</sub> (<i>B</i> = –2.092, <i>p</i> &lt; 0.001), and FEV<sub>1</sub>%/FEV<sub>1</sub>%<sub>predicted</sub> (<i>B</i> = –0.834, <i>p</i> = 0.001). Body mass index (BMI) for age <i>Z</i> score (<i>B</i> = 1.661, <i>p</i> = 0.045) and cesarean delivery (<i>B</i> = 4.471, <i>p</i> = 0.013) were significantly positively correlated with FVC/FVC<sub>predicted</sub>. Birth weight was significantly positively correlated with FEV<sub>1</sub>/FEV<sub>1predicted</sub> (<i>B</i> = 4.593, <i>p</i> = 0.027). Multivariate logistic regression analysis revealed that age ≥6 years and cough variant asthma (CVA) were risk factors for abnormal lung function. Age, BMI for age <i>Z</i> score, mode of delivery, and birth weight were significantly correlated with lung function in children with asthma. Furthermore, children with asthma and normal lung function were more likely to be overlooked. More attention should be given to children with asthma and normal lung function, and CVA.
DOI: 10.6084/m9.figshare.16419179.v1
title: Nano-CuO causes cell damage through activation of dose-dependent autophagy and mitochondrial lncCyt b-AS/ND5-AS/ND6-AS in SH-SY5Y cells

description: Metal copper oxide nanoparticles (nano-CuO) are under mass production and have been widely utilized in many fields including catalysis, gas sensors, semiconductor materials, etc. The broad applications of nano-CuO have increased the possibility of risk to incidental exposure to the environment, and therefore, an in-depth investigation of their effects on live cells is required. This study investigated the impact of the nano-CuO on SH-SY5Y cells, and findings showed that the ratio of LC3-II/LC3-I was significantly increased in SH-SY5Y cells when the cells were treated with nano-CuO. However, if the autophagy inhibitor Bafilomycin A1 (Baf A1) was co-treated, the ratio of LC3-II/LC3-I was further improved. These outcomes might indicate that autophagy flux was permanently elevated by adding nano-CuO. Further results found highly activated levels of long noncoding RNAs (lncRNAs) under nano-CuO treatment. The data illustrate a mechanism that nano-CuO can promote autophagy and activate lncCyt b-AS/ND5-AS/ND6-AS in SH-SY5Y cells and have critical implications for nanoparticle biomedical applications.
DOI: 10.6084/m9.figshare.7505975
title: Additional file 9: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: Table S2. (FASTA 82 kb)
DOI: 10.6084/m9.figshare.13272894
title: GLIPR2 is a negative regulator of autophagy and the BECN1-ATG14-containing phosphatidylinositol 3-kinase complex

description: A key mediator of macroautophagy/autophagy induction is the class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) consisting of PIK3C3/VPS34, PIK3R4/VPS15, BECN1, and ATG14. Although several proteins are known to enhance or decrease PtdIns3K-C1 activity, our understanding of the molecular regulation of PtdIns3K-C1 is still incomplete. Previously, we identified a Golgi-associated protein, GLIPR2, in a screen for proteins that interact with amino acids 267–284 of BECN1, a region of BECN1 sufficient to induce autophagy when fused to a cell penetrating leader sequence. In this study, we used CRISPR-Cas9-mediated depletion of GLIPR2 in cells and mice to investigate the role of GLIPR2 in the regulation of autophagy and PtdIns3K-C1 activity. Depletion of GLIPR2 in HeLa cells increased autelophagic flux and generation of phosphatidylinositol 3-phosphate (PtdIns3P). <i>GLIPR2</i> knockout resulted in less compact Golgi structures, which was also observed in autophagy-inducing conditions such as amino acid starvation or Tat-BECN1 peptide treatment. Importantly, the binding of GLIPR2 to purified PtdIns3K-C1 inhibited the in vitro lipid kinase activity of PtdIns3K-C1. Moreover, the tissues of <i>glipr2</i> knockout mice had increased basal autophagic flux as well as increased recruitment of the PtdIns3P-binding protein, WIPI2. Taken together, our findings demonstrate that GLIPR2 is a negative regulator of PtdIns3K-C1 activity and basal autophagy. <b>Abbreviations:</b> ATG14: autophagy related 14; Baf A1: bafilomycin A<sub>1</sub>; BARA: β-α repeated, autophagy-specific; CQ: chloroquine; GFP: green fluorescent protein; GLIPR2: GLI pathogenesis related 2; HBSS: Hanks’ balanced salt solution; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; PBS: phosphate-buffered saline; PtdIns3K-C1: phosphatidylinositol 3-kinase complex I; PtdIns3P: phosphatidylinositol-3-phosphate; SEM: standard error of the mean; WIPI2: WD repeat domain, phosphoinositide interacting 2
DOI: 10.6084/m9.figshare.20088600
title: Evaluation of the factors affecting lung function in pediatric patients with asthma

description: This study aimed to analyze the risk factors affecting lung function in children with asthma based on clinical data to advice on clinical treatment and prognosis. This study included newly diagnosed patients with asthma admitted to the Respiratory Department of Chengdu Women’s and Children’s Central Hospital in Sichuan from July 2020 to June 2021. The factors associated with lung function were analyzed using univariate and multivariate linear regression with the forward method, while factors affecting lung ventilation function were analyzed using multivariate logistic regression. Sixty percent of the patients had normal lung function. Age was significantly negatively correlated with forced vital capacity (FVC)/FVC<sub>predicted</sub> (<i>B</i> = –1.385, <i>p</i> = 0.001), FEV<sub>1</sub>/FEV<sub>1predicted</sub> (<i>B</i> = –2.092, <i>p</i> &lt; 0.001), and FEV<sub>1</sub>%/FEV<sub>1</sub>%<sub>predicted</sub> (<i>B</i> = –0.834, <i>p</i> = 0.001). Body mass index (BMI) for age <i>Z</i> score (<i>B</i> = 1.661, <i>p</i> = 0.045) and cesarean delivery (<i>B</i> = 4.471, <i>p</i> = 0.013) were significantly positively correlated with FVC/FVC<sub>predicted</sub>. Birth weight was significantly positively correlated with FEV<sub>1</sub>/FEV<sub>1predicted</sub> (<i>B</i> = 4.593, <i>p</i> = 0.027). Multivariate logistic regression analysis revealed that age ≥6 years and cough variant asthma (CVA) were risk factors for abnormal lung function. Age, BMI for age <i>Z</i> score, mode of delivery, and birth weight were significantly correlated with lung function in children with asthma. Furthermore, children with asthma and normal lung function were more likely to be overlooked. More attention should be given to children with asthma and normal lung function, and CVA.
DOI: 10.6084/m9.figshare.13272894.v3
title: GLIPR2 is a negative regulator of autophagy and the BECN1-ATG14-containing phosphatidylinositol 3-kinase complex

description: A key mediator of macroautophagy/autophagy induction is the class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) consisting of PIK3C3/VPS34, PIK3R4/VPS15, BECN1, and ATG14. Although several proteins are known to enhance or decrease PtdIns3K-C1 activity, our understanding of the molecular regulation of PtdIns3K-C1 is still incomplete. Previously, we identified a Golgi-associated protein, GLIPR2, in a screen for proteins that interact with amino acids 267–284 of BECN1, a region of BECN1 sufficient to induce autophagy when fused to a cell penetrating leader sequence. In this study, we used CRISPR-Cas9-mediated depletion of GLIPR2 in cells and mice to investigate the role of GLIPR2 in the regulation of autophagy and PtdIns3K-C1 activity. Depletion of GLIPR2 in HeLa cells increased autelophagic flux and generation of phosphatidylinositol 3-phosphate (PtdIns3P). <i>GLIPR2</i> knockout resulted in less compact Golgi structures, which was also observed in autophagy-inducing conditions such as amino acid starvation or Tat-BECN1 peptide treatment. Importantly, the binding of GLIPR2 to purified PtdIns3K-C1 inhibited the in vitro lipid kinase activity of PtdIns3K-C1. Moreover, the tissues of <i>glipr2</i> knockout mice had increased basal autophagic flux as well as increased recruitment of the PtdIns3P-binding protein, WIPI2. Taken together, our findings demonstrate that GLIPR2 is a negative regulator of PtdIns3K-C1 activity and basal autophagy. <b>Abbreviations:</b> ATG14: autophagy related 14; Baf A1: bafilomycin A<sub>1</sub>; BARA: β-α repeated, autophagy-specific; CQ: chloroquine; GFP: green fluorescent protein; GLIPR2: GLI pathogenesis related 2; HBSS: Hanks’ balanced salt solution; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; PBS: phosphate-buffered saline; PtdIns3K-C1: phosphatidylinositol 3-kinase complex I; PtdIns3P: phosphatidylinositol-3-phosphate; SEM: standard error of the mean; WIPI2: WD repeat domain, phosphoinositide interacting 2