cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.13145/bacdive9569.20221219.7.1
title: Corallococcus coralloides (Thaxter 1892) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9570.20220920.7
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9570.20221219.7.1
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9571.20220920.7
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9571.20221219.7.1
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9572.20220920.7
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9572.20221219.7.1
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9573.20220920.7
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9573.20221219.7.1
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.13145/bacdive9574.20220920.7
title: Corallococcus exiguus (ex Kofler 1913) Reichenbach 2007

description: The range of data encompasses taxonomy, morphology, physiology, sampling and concomitant environmental conditions as well as molecular biology.
DOI: 10.6084/m9.figshare.14913495
title: Additional file 8 of Sex-based clinical and immunological differences in COVID-19

description: Additional file 8: Supplementary Data.
DOI: 10.6084/m9.figshare.12284606.v1
title: Additional file 1 of Impact of coronary collateralization on long-term clinical outcomes in type 2 diabetic patients after successful recanalization of chronic total occlusion

description: Additional file 1: Table S1. Predictors of MACCE and repeat revascularization in all patients on univariable and multivariable analysis.
DOI: 10.6084/m9.figshare.14913423.v1
title: Additional file 11 of The potential roles of m6A modification in regulating the inflammatory response in microglia

description: Additional file 11:. The 87 m6A lncRNAs of hyper methylation M1-L vs M0-L and hypo methylation M2-L vs M1-L
DOI: 10.6084/m9.figshare.14913429.v1
title: Additional file 13 of The potential roles of m6A modification in regulating the inflammatory response in microglia

description: Additional file 13:. The mRNAs differentially expressed between M1-L and M0-L, M2-L and M1-L, and related 43 lncRNAs
DOI: 10.6084/m9.figshare.14913444.v1
title: Additional file 5 of The potential roles of m6A modification in regulating the inflammatory response in microglia

description: Additional file 5:. The mRNA expression level differentially expressed between M1-L and M0-L, M2-L and M1-L
DOI: 10.6084/m9.figshare.14913447
title: Additional file 6 of The potential roles of m6A modification in regulating the inflammatory response in microglia

description: Additional file 6:. The associated analysis of mRNA expression level and methylation level between M1-L and M0-L
DOI: 10.5281/zenodo.10657412
title: Parkinson's Disease GWAS Risk Gene siRNA Knockdown Mitophagy Screen

description: Z-score and B-score calculations for pUb(Ser65) integrated density measurements of PINK1-Parkin dependent mitophagy initiation screen performed in Parkin overexpressing SH-SY5Ys with siRNA KD of Parkinson's Disease risk gene candidates prioritised from Nalls et al., 2019 Parkinson's Disease GWAS meta-analysis.
DOI: 10.5281/zenodo.10657413
title: Parkinson's Disease GWAS Risk Gene siRNA Knockdown Mitophagy Screen

description: Z-score and B-score calculations for pUb(Ser65) integrated density measurements of PINK1-Parkin dependent mitophagy initiation screen performed in Parkin overexpressing SH-SY5Ys with siRNA KD of Parkinson's Disease risk gene candidates prioritised from Nalls et al., 2019 Parkinson's Disease GWAS meta-analysis.
DOI: 10.6084/m9.figshare.14905996
title: Additional file 3 of Comparative analyses of the Hymenoscyphus fraxineus and Hymenoscyphus albidus genomes reveals potentially adaptive differences in secondary metabolite and transposable element repertoires

description: Additional file 3:
DOI: 10.6084/m9.figshare.14905999
title: Additional file 4 of Comparative analyses of the Hymenoscyphus fraxineus and Hymenoscyphus albidus genomes reveals potentially adaptive differences in secondary metabolite and transposable element repertoires

description: Additional file 4:
DOI: 10.6084/m9.figshare.13340752.v3
title: Autophagy alleviates hypoxia-induced blood-brain barrier injury via regulation of CLDN5 (claudin 5)

description: Blood-brain barrier (BBB) disruption is a key event in triggering secondary damage to the central nervous system (CNS) under stroke, and is frequently associated with abnormal macroautophagy/autophagy in brain microvascular endothelial cells (BMECs). However, the underlying mechanism of autophagy in maintaining BBB integrity remains unclear. Here we report that in BMECs of patients suffering stroke, CLDN5 (claudin 5) abnormally aggregates in the cytosol accompanied by autophagy activation. <i>In vivo</i> zebrafish and <i>in vitro</i> cell studies reveal that BBB breakdown is partially caused by CAV1 (caveolin 1)-mediated redistribution of membranous CLDN5 into the cytosol under hypoxia. Meanwhile, autophagy is activated and contributes mainly to the degradation of CAV1 and aggregated CLDN5 in the cytosol of BMECs, therefore alleviating BBB breakdown. Blockage of autophagy by genetic methods or chemicals aggravates cytosolic aggregation of CLDN5, resulting in severer BBB impairment. These data demonstrate that autophagy functions in the protection of BBB integrity by regulating CLDN5 redistribution and provide a potential therapeutic strategy for BBB disorder-related cerebrovascular disease. <b>Abbreviations:</b> BBB: blood-brain barrier; BECN1: beclin 1; BMEC: brain microvascular endothelial cell; CAV1: caveolin 1; CCA: common carotid artery; CLDN5: claudin 5; CNS: central nervous system; CQ: chloroquine; HIF1A: hypoxia inducible factor 1 subunit alpha; MCAO: middle cerebral artery occlusion-reperfusion; OCLN: occludin; ROS: reactive oxygen species; STED: stimulated emission depletion; TEER: trans-endothelial electrical resistance; TEM: transmission electron microscopy; TJ: tight junction; TJP1: tight junction protein 1; UPS: ubiquitin-proteasome system
DOI: 10.25387/g3.12816482
title: Supplemental Material for Miller et al., 2020

description: Figure S1 is the Epistatic interaction between loci on chromosome 6 regulate red cell distribution width in blood. Figure S2 Main Effect mRNA Expression of Extl1 and Cadps2. Figure S3 is Interaction Effect mRNA Expression of Tmem245.Table S1 is the raw genotype data, S2 is the raw trait data file, S5 is the RNA seq main effects results, S6 is the RNA Seq Interaction results, and S7 is the gene ontology.
DOI: 10.6084/m9.figshare.14913582
title: Additional file 1 of Integration of transcriptomic data identifies key hallmark genes in hypertrophic cardiomyopathy

description: Additional file 1. Table S1: The statistical information of the 48 DEGs obtained in microarray dataset. Table S2: The statistical information of the 48 DEGs obtained in RNA-Seq dataset. Table S3: Results of the three classifiers for both accuracy and f1-score when using different numbers of genes.
DOI: 10.6084/m9.figshare.14913582.v1
title: Additional file 1 of Integration of transcriptomic data identifies key hallmark genes in hypertrophic cardiomyopathy

description: Additional file 1. Table S1: The statistical information of the 48 DEGs obtained in microarray dataset. Table S2: The statistical information of the 48 DEGs obtained in RNA-Seq dataset. Table S3: Results of the three classifiers for both accuracy and f1-score when using different numbers of genes.
DOI: 10.6084/m9.figshare.13340752.v1
title: Autophagy alleviates hypoxia-induced blood-brain barrier injury via regulation of CLDN5 (claudin 5)

description: Blood-brain barrier (BBB) disruption is a key event in triggering secondary damage to the central nervous system (CNS) under stroke, and is frequently associated with abnormal macroautophagy/autophagy in brain microvascular endothelial cells (BMECs). However, the underlying mechanism of autophagy in maintaining BBB integrity remains unclear. Here we report that in BMECs of patients suffering stroke, CLDN5 (claudin 5) abnormally aggregates in the cytosol accompanied by autophagy activation. <i>In vivo</i> zebrafish and <i>in vitro</i> cell studies reveal that BBB breakdown is partially caused by CAV1 (caveolin 1)-mediated redistribution of membranous CLDN5 into the cytosol under hypoxia. Meanwhile, autophagy is activated and contributes mainly to the degradation of CAV1 and aggregated CLDN5 in the cytosol of BMECs, therefore alleviating BBB breakdown. Blockage of autophagy by genetic methods or chemicals aggravates cytosolic aggregation of CLDN5, resulting in severer BBB impairment. These data demonstrate that autophagy functions in the protection of BBB integrity by regulating CLDN5 redistribution and provide a potential therapeutic strategy for BBB disorder-related cerebrovascular disease. <b>Abbreviations:</b> BBB: blood-brain barrier; BECN1: beclin 1; BMEC: brain microvascular endothelial cell; CAV1: caveolin 1; CCA: common carotid artery; CLDN5: claudin 5; CNS: central nervous system; CQ: chloroquine; HIF1A: hypoxia inducible factor 1 subunit alpha; MCAO: middle cerebral artery occlusion-reperfusion; OCLN: occludin; ROS: reactive oxygen species; STED: stimulated emission depletion; TEER: trans-endothelial electrical resistance; TEM: transmission electron microscopy; TJ: tight junction; TJP1: tight junction protein 1; UPS: ubiquitin-proteasome system
DOI: 10.6084/m9.figshare.13340752.v2
title: Autophagy alleviates hypoxia-induced blood-brain barrier injury via regulation of CLDN5 (claudin 5)

description: Blood-brain barrier (BBB) disruption is a key event in triggering secondary damage to the central nervous system (CNS) under stroke, and is frequently associated with abnormal macroautophagy/autophagy in brain microvascular endothelial cells (BMECs). However, the underlying mechanism of autophagy in maintaining BBB integrity remains unclear. Here we report that in BMECs of patients suffering stroke, CLDN5 (claudin 5) abnormally aggregates in the cytosol accompanied by autophagy activation. <i>In vivo</i> zebrafish and <i>in vitro</i> cell studies reveal that BBB breakdown is partially caused by CAV1 (caveolin 1)-mediated redistribution of membranous CLDN5 into the cytosol under hypoxia. Meanwhile, autophagy is activated and contributes mainly to the degradation of CAV1 and aggregated CLDN5 in the cytosol of BMECs, therefore alleviating BBB breakdown. Blockage of autophagy by genetic methods or chemicals aggravates cytosolic aggregation of CLDN5, resulting in severer BBB impairment. These data demonstrate that autophagy functions in the protection of BBB integrity by regulating CLDN5 redistribution and provide a potential therapeutic strategy for BBB disorder-related cerebrovascular disease. <b>Abbreviations:</b> BBB: blood-brain barrier; BECN1: beclin 1; BMEC: brain microvascular endothelial cell; CAV1: caveolin 1; CCA: common carotid artery; CLDN5: claudin 5; CNS: central nervous system; CQ: chloroquine; HIF1A: hypoxia inducible factor 1 subunit alpha; MCAO: middle cerebral artery occlusion-reperfusion; OCLN: occludin; ROS: reactive oxygen species; STED: stimulated emission depletion; TEER: trans-endothelial electrical resistance; TEM: transmission electron microscopy; TJ: tight junction; TJP1: tight junction protein 1; UPS: ubiquitin-proteasome system
DOI: 10.6084/m9.figshare.13340752
title: Autophagy alleviates hypoxia-induced blood-brain barrier injury via regulation of CLDN5 (claudin 5)

description: Blood-brain barrier (BBB) disruption is a key event in triggering secondary damage to the central nervous system (CNS) under stroke, and is frequently associated with abnormal macroautophagy/autophagy in brain microvascular endothelial cells (BMECs). However, the underlying mechanism of autophagy in maintaining BBB integrity remains unclear. Here we report that in BMECs of patients suffering stroke, CLDN5 (claudin 5) abnormally aggregates in the cytosol accompanied by autophagy activation. <i>In vivo</i> zebrafish and <i>in vitro</i> cell studies reveal that BBB breakdown is partially caused by CAV1 (caveolin 1)-mediated redistribution of membranous CLDN5 into the cytosol under hypoxia. Meanwhile, autophagy is activated and contributes mainly to the degradation of CAV1 and aggregated CLDN5 in the cytosol of BMECs, therefore alleviating BBB breakdown. Blockage of autophagy by genetic methods or chemicals aggravates cytosolic aggregation of CLDN5, resulting in severer BBB impairment. These data demonstrate that autophagy functions in the protection of BBB integrity by regulating CLDN5 redistribution and provide a potential therapeutic strategy for BBB disorder-related cerebrovascular disease. <b>Abbreviations:</b> BBB: blood-brain barrier; BECN1: beclin 1; BMEC: brain microvascular endothelial cell; CAV1: caveolin 1; CCA: common carotid artery; CLDN5: claudin 5; CNS: central nervous system; CQ: chloroquine; HIF1A: hypoxia inducible factor 1 subunit alpha; MCAO: middle cerebral artery occlusion-reperfusion; OCLN: occludin; ROS: reactive oxygen species; STED: stimulated emission depletion; TEER: trans-endothelial electrical resistance; TEM: transmission electron microscopy; TJ: tight junction; TJP1: tight junction protein 1; UPS: ubiquitin-proteasome system
DOI: 10.25387/g3.12816482.v1
title: Supplemental Material for Miller et al., 2020

description: Figure S1 is the Epistatic interaction between loci on chromosome 6 regulate red cell distribution width in blood. Figure S2 Main Effect mRNA Expression of Extl1 and Cadps2. Figure S3 is Interaction Effect mRNA Expression of Tmem245.Table S1 is the raw genotype data, S2 is the raw trait data file, S5 is the RNA seq main effects results, S6 is the RNA Seq Interaction results, and S7 is the gene ontology.
DOI: 10.6084/m9.figshare.14913576
title: Additional file 1 of Utility of interferon gamma/tumor necrosis factor alpha FluoroSpot assay in differentiation between active tuberculosis and latent tuberculosis infection: a pilot study

description: Additional file 1 Supplementary Table 1. Frequencies of single TNF-α-, total TNF-α-, single IFN-γ-, total IFN-γ-, dual IFN-γ/TNF-α-secreting T cells following ESAT-6 or/and CFP-10 stimulation in ATB, LTBI and HC groups. Supplementary Table 2. Frequencies of spot-forming T cell in nil control in ATB, LTBI and HC groups. Supplementary Table 3. Diagnostic accuracy of single TNF-α-, total TNF-α-, single IFN-γ-, total IFN-γ-, dual IFN-γ/TNF-α-secreting T cells following ESAT-6 or/and CFP-10 stimulation in differentiating ATB and LTBI.
DOI: 10.6084/m9.figshare.14913519.v1
title: Additional file 3 of Integrative analysis of ceRNA network reveals functional lncRNAs associated with independent recurrent prognosis in colon adenocarcinoma

description: Additional file 3: Table S2. Screening of connection pairs between 4 DEmiRNAs and selected DEmRNAs predicted by (TargetScan, PicTar, RNA22, Pita and MIRANDA).
DOI: 10.6084/m9.figshare.14913630
title: Additional file 5 of GA3 is superior to GA4 in promoting bud endodormancy release in tree peony (Paeonia suffruticosa) and their potential working mechanism

description: Additional file 5: The transcriptomic data of the overlapping 849 DEGs between GA3 vs GA4 and GA3 vs mock, GA3 vs GA4 and GA4 vs mock, respectively.
DOI: 10.6084/m9.figshare.25218920
title: test_data

description: NWP data with random noise added.
DOI: 10.6084/m9.figshare.25218920.v1
title: test_data

description: NWP data with random noise added.
DOI: 10.6084/m9.figshare.24754149
title: Data&Code availability

description: coherence time series dataset, results of assessment
DOI: 10.6084/m9.figshare.24754149.v1
title: Data availability

description: coherence time series dataset, results of assessment
DOI: 10.6084/m9.figshare.14913768
title: Additional file 13 of Nuclear Transglutaminase 2 interacts with topoisomerase II⍺ to promote DNA damage repair in lung cancer cells

description: Additional file 13.
DOI: 10.6084/m9.figshare.14913795
title: Additional file 8 of Nuclear Transglutaminase 2 interacts with topoisomerase II⍺ to promote DNA damage repair in lung cancer cells

description: Additional file 8.
DOI: 10.6084/m9.figshare.14913765
title: Additional file 12 of Nuclear Transglutaminase 2 interacts with topoisomerase II⍺ to promote DNA damage repair in lung cancer cells

description: Additional file 12.
DOI: 10.6084/m9.figshare.14913798.v1
title: Additional file 9 of Nuclear Transglutaminase 2 interacts with topoisomerase II⍺ to promote DNA damage repair in lung cancer cells

description: Additional file 9.
DOI: 10.4121/858870bc-ce57-4782-8ee6-48cfd171db63.v1
title: Data underlying the publication: High-throughput mechanophenotyping of multicellular spheroids using a microfluidic micropipette aspiration chip

description: Research paper published in Lab on a Chip, on the development of a microfluidic chip that allows high-throughput aspiration of multicellular spheroids to characterize tissue mechanics. Data includes Excel files with measured spheroid mechanical parameters such as their elasticity and viscosity. Additionally, the Python codes used for analysis and the AutoCAD files including the microfluidic chip designs are included.
DOI: 10.6084/m9.figshare.14913795.v1
title: Additional file 8 of Nuclear Transglutaminase 2 interacts with topoisomerase II⍺ to promote DNA damage repair in lung cancer cells

description: Additional file 8.
DOI: 10.6084/m9.figshare.20156812
title: Additional file 1 of Identification and expression analysis of GARP superfamily genes in response to nitrogen and phosphorus stress in Spirodela polyrhiza

description: Additional file 1: Table S1. List of GARP superfamily members identified genome-wide in Colocasia esculenta and Wolffia Australiana. Table S2. The Ka/Ks and divergence time of SpGARP paralogs and orthologs gene pairs. Table S3. The frequency of 245 cis-regulatory elements in the 2000 bp promoter region of GARP genes in giant duckweed, scanned in New PLACE database. Table S4. Primer sequences used in qRT-PCR.
DOI: 10.6084/m9.figshare.14913798
title: Additional file 9 of Nuclear Transglutaminase 2 interacts with topoisomerase II⍺ to promote DNA damage repair in lung cancer cells

description: Additional file 9.
DOI: 10.6084/m9.figshare.14913752
title: Additional file 2 of Identification of potential biomarkers for pathogenesis of Alzheimer’s disease

description: Additional file 2. The clinical characteristics of samples in GSE63060 and GSE140829 datasets.
DOI: 10.6084/m9.figshare.14913765.v1
title: Additional file 12 of Nuclear Transglutaminase 2 interacts with topoisomerase II⍺ to promote DNA damage repair in lung cancer cells

description: Additional file 12.
DOI: 10.6084/m9.figshare.14913752.v1
title: Additional file 2 of Identification of potential biomarkers for pathogenesis of Alzheimer’s disease

description: Additional file 2. The clinical characteristics of samples in GSE63060 and GSE140829 datasets.
DOI: 10.6084/m9.figshare.14913768.v1
title: Additional file 13 of Nuclear Transglutaminase 2 interacts with topoisomerase II⍺ to promote DNA damage repair in lung cancer cells

description: Additional file 13.
DOI: 10.6084/m9.figshare.20156812.v1
title: Additional file 1 of Identification and expression analysis of GARP superfamily genes in response to nitrogen and phosphorus stress in Spirodela polyrhiza

description: Additional file 1: Table S1. List of GARP superfamily members identified genome-wide in Colocasia esculenta and Wolffia Australiana. Table S2. The Ka/Ks and divergence time of SpGARP paralogs and orthologs gene pairs. Table S3. The frequency of 245 cis-regulatory elements in the 2000 bp promoter region of GARP genes in giant duckweed, scanned in New PLACE database. Table S4. Primer sequences used in qRT-PCR.
DOI: 10.6084/m9.figshare.20681048.v1
title: Stress-dependent design and optimization methodology of gradient porous implant and application in femoral stem

description: Gradient porous structure made by additive manufacturing (AM) technology is potential to improve the long-term stability of orthopaedic implants through bone ingrowth while maintaining mechanical safety. In this study, a parametrical optimization methodology for the customized gradient porous implants was developed based on a stress-dependent design algorithm. Clinical requirements and manufacturing capabilities of AM were considered in the design procedure. A femoral stem with a minimum bone loss proportion of 2.4% by optimizing the control parameters. This study provided a feasible and flexible design approach for the customized implant with gradient porous structure or material components.
DOI: 10.6084/m9.figshare.20681048
title: Stress-dependent design and optimization methodology of gradient porous implant and application in femoral stem

description: Gradient porous structure made by additive manufacturing (AM) technology is potential to improve the long-term stability of orthopaedic implants through bone ingrowth while maintaining mechanical safety. In this study, a parametrical optimization methodology for the customized gradient porous implants was developed based on a stress-dependent design algorithm. Clinical requirements and manufacturing capabilities of AM were considered in the design procedure. A femoral stem with a minimum bone loss proportion of 2.4% by optimizing the control parameters. This study provided a feasible and flexible design approach for the customized implant with gradient porous structure or material components.
DOI: 10.6084/m9.figshare.20681032
title: Paenibacillus dendrobii sp. nov., an indole-3-acetic acid-producing endophytic bacterium isolated from Dendrobium nobile

description: Supplementary Material for ‘Paenibacillus dendrobii sp. nov., an indole-3-acetic acid-producing endophytic bacterium isolated from Dendrobium nobile’, as published in International Journal of Systematic and Evolutionary Microbiology.
DOI: 10.5281/zenodo.10566416
title: RadWet-L ALOS-2 PALSAR-2 ScanSAR Orbit Cycle Classified Products 2019-2023
DOI: 10.5281/zenodo.10566417
title: RadWet-L ALOS-2 PALSAR-2 ScanSAR Orbit Cycle Classified Products 2019-2023
DOI: 10.6084/m9.figshare.20681032.v1
title: Paenibacillus dendrobii sp. nov., an indole-3-acetic acid-producing endophytic bacterium isolated from Dendrobium nobile

description: Supplementary Material for ‘Paenibacillus dendrobii sp. nov., an indole-3-acetic acid-producing endophytic bacterium isolated from Dendrobium nobile’, as published in International Journal of Systematic and Evolutionary Microbiology.