cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7992590.v1
title: CCDB_3754.jpg

description: Projection through merged optical section series of a filled astrocyte (green) in the molecular layer of the dentate gyrus, stained for Epha4 (red), showing the relationship between astrocyte processes and laminar boundaries revealed by EphA4 staining.
DOI: 10.6084/m9.figshare.7992578
title: CCDB_3751.jpg

description: Projection through merged optical section series of a filled astrocyte (green) in the molecular layer of the dentate gyrus, stained for Epha4 (red), showing the relationship between astrocyte processes and laminar boundaries revealed by EphA4 staining.
DOI: 10.6084/m9.figshare.7992581
title: CCDB_3752.jpg

description: Projection through merged optical section series of a filled astrocyte (green) in the molecular layer of the dentate gyrus, stained for Epha4 (red), showing the relationship between astrocyte processes and laminar boundaries revealed by EphA4 staining.
DOI: 10.6084/m9.figshare.7992587.v1
title: CCDB_3753.jpg

description: Projection through merged optical section series of a filled astrocyte (green) in the molecular layer of the dentate gyrus, stained for Epha4 (red), showing the relationship between astrocyte processes and laminar boundaries revealed by EphA4 staining.
DOI: 10.6084/m9.figshare.7992578.v1
title: CCDB_3751.jpg

description: Projection through merged optical section series of a filled astrocyte (green) in the molecular layer of the dentate gyrus, stained for Epha4 (red), showing the relationship between astrocyte processes and laminar boundaries revealed by EphA4 staining.
DOI: 10.6084/m9.figshare.7992581.v1
title: CCDB_3752.jpg

description: Projection through merged optical section series of a filled astrocyte (green) in the molecular layer of the dentate gyrus, stained for Epha4 (red), showing the relationship between astrocyte processes and laminar boundaries revealed by EphA4 staining.
DOI: 10.6084/m9.figshare.7992572
title: Towards the integration of animal-borne instruments into global ocean observing systems

description: The following supplement accompanies the article:March, D, Boehme, L, Tintoré, J, Vélez‐Belchi, PJ, Godley, BJ. Towards the integration of animal‐borne instruments into global ocean observing systems. Glob Change Biol. 2019; 00: 1– 11. https://doi.org/10.1111/gcb.14902<br><br><b><br></b><b>Supplementary Data 1</b> Filename: sd1_tbl_species_list.csv Description: Table containing the list of 183 marine vertebrate species.<br> <b>Supplementary Data 2</b> Filename: sd2_tbl_overlap_results.csv Description: Table containing the overlap indices for all combinations of species and data types (i.e. 183 species from EOO maps and 17 species from Telemetry data), and ocean regions (ie. Northern Ocean, Tropical Ocean, Southern Ocean, Artic Ocean, Antarctic Ocean and Global Ocean).<br> <b>Supplementary Data 3</b> Filename: sd3_argo_gap_persistence.nc Description: Map of the Argo gap persistence <b>Supplementary Data 4</b> Filename: sd4_argo_coldspots.nc Description: Map of the Argo coldspots<br> <b>Supplementary Data 5</b> Filename: sd5_eoo_species_per_group.zip Description: Density maps of species subject to telemetry by taxonomic group based on EOO maps<br> <b>Supplementary Data 6</b> Filename: sd6_telemetry_dens_per_group.zip Description: Density maps of telemetry observations by taxonomic group
DOI: 10.6084/m9.figshare.7992566
title: Interactive non-fiction projects 2010-2018

description: A database of 524 works of interactive non-fiction (2010-2018): interactive documentary, VR, AR, multimedia reportage, installations, etc.
DOI: 10.6084/m9.figshare.7992539
title: The Visibility of Translation in the Context of Sam Tung Uk, perpared by Goal Diggers

description: The fileset presents a case study of museum representations in Sam Tung Uk Museum, Hong Kong. <br> The data are collected by the authors on a field trip to the Museum dated 28 March 2019.<br> The fileset includes:1. A compilation of all immediately accessible Chinese texts in the museum, namely C-text.docx; 2. A compilation of all immediately accessible English texts in the museum, namely E-text docx;<br>3. Word cloud of English tiles, namely E-cloud.jpg;<br>4. Word cloud of Chinese tiles, namely C-cloud.jpg; and<br>5. Analysis, namely The Analysis.docx.<br><br>The fileset is uploaded on 15 April 2019 for assessment in TRAN4210 Translation Criticism, an advanced course offered by Department of Translation, Chinese University of Hong Kong, in the academic year 2018-19. <br><br>
DOI: 10.6084/m9.figshare.7992566.v2
title: Interactive non-fiction projects 2010-2018

description: A database of 524 works of interactive non-fiction (2010-2018): interactive documentary, VR, AR, multimedia reportage, installations, etc.
DOI: 10.6084/m9.figshare.7992566.v1
title: Interactive non-fiction projects 2010-2018

description: A database of 524 works of interactive non-fiction (2010-2018): interactive documentary, VR, AR, multimedia reportage, installations, etc. It is a result of the PhD dissertation of the author.
DOI: 10.6084/m9.figshare.7992539.v2
title: The Visibility of Translation in the Context of Sam Tung Uk, perpared by Goal Diggers

description: The fileset presents a case study of museum representations in Sam Tung Uk Museum, Hong Kong. <br> The data are collected by the authors on a field trip to the Museum dated 28 March 2019.<br> The fileset includes:1. A compilation of all immediately accessible Chinese texts in the museum, namely C-text.docx; 2. A compilation of all immediately accessible English texts in the museum, namely E-text docx;<br>3. Word cloud of English tiles, namely E-cloud.jpg;<br>4. Word cloud of Chinese tiles, namely C-cloud.jpg; and<br>5. Analysis, namely The Analysis.docx.<br><br>The fileset is uploaded on 15 April 2019 for assessment in TRAN4210 Translation Criticism, an advanced course offered by Department of Translation, Chinese University of Hong Kong, in the academic year 2018-19. <br><br>
DOI: 10.6084/m9.figshare.7992539.v1
title: The Visibility of Translation in the Context of Sam Tung Uk, perpared by Goal Diggers

description: The fileset presents a case study of museum representations in Sam Tung Uk Museum, Hong Kong. <br> The data are collected by the authors on a field trip to the Museum dated 28 March 2019.<br> The fileset includes: <br>1. A compilation of all immediately accessible Chinese texts in the museum, namely C-text.docx; <br>2. A compilation of all immediately accessible English texts in the museum, namely E-text docx;<br>3. Word cloud of English tiles, namely E-cloud.jpg;<br>4. Word cloud of Chinese tiles, namely C-cloud.jpg; and<br>5. Analysis, namely The Analysis.docx.<br>The fileset is uploaded on 15 April 2019 for assessment in TRAN4210 Translation Criticism, an advanced course offered by Department of Translation, Chinese University of Hong Kong, in the academic year 2018-19. <br><br>
DOI: 10.6084/m9.figshare.7992500
title: The negative effect of lipid challenge on autophagy inhibits T cell responses

description: Obesity is associated with changes in the immune system that significantly hinder its ability to mount efficient immune responses. Previous studies have reported a dysregulation of immune responses caused by lipid challenge; however, the mechanisms underlying that dysregulation are still not completely understood. Autophagy is an essential catabolic process through which cellular components are degraded by the lysosomal machinery. In T cells, autophagy is an actively regulated process necessary to sustain homeostasis and activation. Here, we report that CD4<sup>+</sup> T cell responses are inhibited when cells are challenged with increasing concentrations of fatty acids. Furthermore, analysis of T cells from diet-induced obese mice confirms that high lipid load inhibits activation-induced responses in T cells. We have found that autophagy is inhibited in CD4<sup>+</sup> T cells exposed <i>in vitro</i> or <i>in vivo</i> to lipid stress, which causes decreased autophagosome formation and degradation. Supporting that inhibition of autophagy caused by high lipid load is a key mechanism that accounts for the effects on T cell function of lipid stress, we found that ATG7 (autophagy-related 7)-deficient T cells, unable to activate autophagy, did not show additional inhibitory effects on their responses to activation when subjected to lipid challenge. Our results indicate, thus, that increased lipid load can dysregulate autophagy and cause defective T cell responses, and suggest that inhibition of autophagy may underlie some of the characteristic obesity-associated defects in the T cell compartment. <b>Abbreviations</b>: ACTB: actin, beta; ATG: autophagy-related; CDKN1B: cyclin-dependent kinase inhibitor 1B; HFD: high-fat diet; IFNG: interferon gamma; IL: interleukin; MAPK1/ERK2: mitogen-activated protein kinase 1; MAPK3/ERK1: mitogen-activated protein kinase 3; MAPK8/JNK: mitogen-activated protein kinase 8; LC3-I: non-conjugated form of MAP1LC3B; LC3-II: phosphatidylethanolamine-conjugated form of MAP1LC3B; MAP1LC3B: microtubule-associated protein 1 light chain 3 beta; MS: mass spectrometry; MTOR: mechanistic target of rapamycin kinase; NFATC2: nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 2; NLRP3: NLR family, pyrin domain containing 3; OA: oleic acid; PI: propidium iodide; ROS: reactive oxygen species; STAT5A: signal transducer and activator of transcription 5A; TCR: T cell receptor; T<sub>H</sub>1: T helper cell type 1
DOI: 10.6084/m9.figshare.7992497
title: Appendix 1. Information samples in this study and previous papers- Mediterranean ancestral area and recent historical events of the white wagtail, Motacilla alba (Passeriformes: Motacillidae), complex

description: <i>Contributions to Zoology</i> <b>Mediterranean ancestral area and recent historical events of the white wagtail, <i>Motacilla alba </i>(Passeriformes: Motacillidae), complex</b> <b>Maliheh Pirayesh Shirazinejad, Mansour Aliabadian<sup>*</sup> and Omid Mirshamsi</b> <b> </b> Appendix 1: Information samples in this study and previous papers
DOI: 10.6084/m9.figshare.7992497.v1
title: Appendix 1. Information samples in this study and previous papers- Mediterranean ancestral area and recent historical events of the white wagtail, Motacilla alba (Passeriformes: Motacillidae), complex

description: <i>Contributions to Zoology</i> <b>Mediterranean ancestral area and recent historical events of the white wagtail, <i>Motacilla alba </i>(Passeriformes: Motacillidae), complex</b> <b>Maliheh Pirayesh Shirazinejad, Mansour Aliabadian<sup>*</sup> and Omid Mirshamsi</b> <b> </b> Appendix 1: Information samples in this study and previous papers
DOI: 10.6084/m9.figshare.7992500.v2
title: The negative effect of lipid challenge on autophagy inhibits T cell responses

description: Obesity is associated with changes in the immune system that significantly hinder its ability to mount efficient immune responses. Previous studies have reported a dysregulation of immune responses caused by lipid challenge; however, the mechanisms underlying that dysregulation are still not completely understood. Autophagy is an essential catabolic process through which cellular components are degraded by the lysosomal machinery. In T cells, autophagy is an actively regulated process necessary to sustain homeostasis and activation. Here, we report that CD4<sup>+</sup> T cell responses are inhibited when cells are challenged with increasing concentrations of fatty acids. Furthermore, analysis of T cells from diet-induced obese mice confirms that high lipid load inhibits activation-induced responses in T cells. We have found that autophagy is inhibited in CD4<sup>+</sup> T cells exposed <i>in vitro</i> or <i>in vivo</i> to lipid stress, which causes decreased autophagosome formation and degradation. Supporting that inhibition of autophagy caused by high lipid load is a key mechanism that accounts for the effects on T cell function of lipid stress, we found that ATG7 (autophagy-related 7)-deficient T cells, unable to activate autophagy, did not show additional inhibitory effects on their responses to activation when subjected to lipid challenge. Our results indicate, thus, that increased lipid load can dysregulate autophagy and cause defective T cell responses, and suggest that inhibition of autophagy may underlie some of the characteristic obesity-associated defects in the T cell compartment. <b>Abbreviations</b>: ACTB: actin, beta; ATG: autophagy-related; CDKN1B: cyclin-dependent kinase inhibitor 1B; HFD: high-fat diet; IFNG: interferon gamma; IL: interleukin; MAPK1/ERK2: mitogen-activated protein kinase 1; MAPK3/ERK1: mitogen-activated protein kinase 3; MAPK8/JNK: mitogen-activated protein kinase 8; LC3-I: non-conjugated form of MAP1LC3B; LC3-II: phosphatidylethanolamine-conjugated form of MAP1LC3B; MAP1LC3B: microtubule-associated protein 1 light chain 3 beta; MS: mass spectrometry; MTOR: mechanistic target of rapamycin kinase; NFATC2: nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 2; NLRP3: NLR family, pyrin domain containing 3; OA: oleic acid; PI: propidium iodide; ROS: reactive oxygen species; STAT5A: signal transducer and activator of transcription 5A; TCR: T cell receptor; T<sub>H</sub>1: T helper cell type 1
DOI: 10.6084/m9.figshare.7992457
title: Age-dependent accumulation of oligomeric SNCA/α-synuclein from impaired degradation in mutant LRRK2 knockin mouse model of Parkinson disease: role for therapeutic activation of chaperone-mediated autophagy (CMA)

description: Parkinson disease (PD) is an age-related neurodegenerative disorder associated with misfolded SNCA/α-synuclein accumulation in brain. Impaired catabolism of SNCA potentiates formation of its toxic oligomers. <i>LRRK2</i> (leucine-rich repeat kinase-2) mutations predispose to familial and sporadic PD. Mutant LRRK2 perturbs chaperone-mediated-autophagy (CMA) to degrade SNCA. We showed greater age-dependent accumulation of oligomeric SNCA in striatum and cortex of aged LRRK2<sup>R1441G</sup> knockin (KI) mice, compared to age-matched wildtype (WT) by 53% and 31%, respectively. Lysosomal clustering and accumulation of CMA-specific LAMP2A and HSPA8/HSC70 proteins were observed in aged mutant striatum along with increased GAPDH (CMA substrate) by immunohistochemistry of dorsal striatum and flow cytometry of ventral midbrain cells. Using our new reporter protein clearance assay, mutant mouse embryonic fibroblasts (MEFs) expressing either SNCA or CMA recognition ‘KFERQ’-like motif conjugated with photoactivated-PAmCherry showed slower cellular clearance compared to WT by 28% and 34%, respectively. However, such difference was not observed after the ‘KFERQ’-motif was mutated. LRRK2 mutant MEFs exhibited lower lysosomal degradation than WT indicating lysosomal dysfunction. LAMP2A-knockdown reduced total lysosomal activity and clearance of ‘KFERQ’-substrate in WT but not in mutant MEFs, indicating impaired CMA in the latter. A CMA-specific activator, AR7, induced neuronal LAMP2A transcription and lysosomal activity in MEFs. AR7 also attenuated the progressive accumulation of both intracellular and extracellular SNCA oligomers in prolonged cultures of mutant cortical neurons (DIV21), indicating that oligomer accumulation can be suppressed by CMA activation. Activation of autophagic pathways to reduce aged-related accumulation of pathogenic SNCA oligomers is a viable disease-modifying therapeutic strategy for PD. <b>Abbreviations:</b> 3-MA: 3-methyladenine; AR7: 7-chloro-3-(4-methylphenyl)-2H-1,4-benzoxazine; CMA: chaperone-mediated autophagy; CQ: chloroquine; CSF: cerebrospinal fluid; DDM: n-dodecyl β-D-maltoside; DIV: days in vitro; ELISA: enzyme-linked immunosorbent assay; FACS: fluorescence-activated cell sorting; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GWAS: genome-wide association studies; HSPA8/HSC70: heat shock protein 8; KFERQ: CMA recognition pentapeptide; KI: knockin; LAMP1: lysosomal-associated membrane protein 1; LAMP2A: lysosomal-associated membrane protein 2A; LDH: lactate dehydrogenase; LRRK2: leucine-rich repeat kinase 2; MEF: mouse embryonic fibroblast; NDUFS4: NADH:ubiquinone oxidoreductase core subunit S4; NE: novel epitope; PD: Parkinson disease; RARA/RARα: retinoic acid receptor, alpha; SNCA: synuclein, alpha; TUBB3/TUJ1: tubulin, beta 3 class III; WT: wild-type
DOI: 10.6084/m9.figshare.7992500.v1
title: The negative effect of lipid challenge on autophagy inhibits T cell responses

description: Obesity is associated with changes in the immune system that significantly hinder its ability to mount efficient immune responses. Previous studies have reported a dysregulation of immune responses caused by lipid challenge; however, the mechanisms underlying that dysregulation are still not completely understood. Autophagy is an essential catabolic process through which cellular components are degraded by the lysosomal machinery. In T cells, autophagy is an actively regulated process necessary to sustain homeostasis and activation. Here, we report that CD4<sup>+</sup> T cell responses are inhibited when cells are challenged with increasing concentrations of fatty acids. Furthermore, analysis of T cells from diet-induced obese mice confirms that high lipid load inhibits activation-induced responses in T cells. We have found that autophagy is inhibited in CD4<sup>+</sup> T cells exposed <i>in vitro</i> or <i>in vivo</i> to lipid stress, which causes decreased autophagosome formation and degradation. Supporting that inhibition of autophagy caused by high lipid load is a key mechanism that accounts for the effects on T cell function of lipid stress, we show that ATG7 (autophagy-related 7)-deficient T cells, unable to activate autophagy, did not show additional inhibitory effects on their responses to activation when subjected to lipid challenge. Our results indicate, thus, that increased lipid load can dysregulate autophagy and cause defective T cell responses, and suggest that inhibition of autophagy may underlie some of the characteristic obesity-associated defects in the T cell compartment.
DOI: 10.6084/m9.figshare.7992313
title: Effects of compressive ratio and sintering temperature on mechanical properties of biocompatible collagen/hydroxyapatite composite scaffolds fabricated for bone tissue engineering

description: A sponge template method was used to synthesize scaffolds from hydroxyapatite (HAp) using varying sintering temperatures and compressive ratios. The HAp scaffolds were fabricated with collagen (COL) or collagen/HAp particles under room temperature coating conditions. The microstructure and mechanical properties of the fabricated biomaterials were analyzed by FE-SEM and EZ Test, respectively. The FE-SEM micrographs showed microporous structure of the fabricated composite scaffolds. Incorporation of COL or COL/HAp into pure HAp scaffolds under coating conditions significantly reduced the porosity and enhanced the mechanical properties. The results demonstrated that the porosity of fabricated scaffolds was reduced by lowering the compressive pressure and increasing the sintering temperature. The maximum estimated compressive moduli at 1000, 1100 and 1200 °C for HAp-COL and HAp-COL/HAp composite scaffolds were 4.36, 2.93, 5.09 MPa and 4.57, 8.19, 5.02 MPa, respectively, at a 50% compressive ratio. It was assumed that porosity was effectively reduced to the maximum level at a 50% compressive ratio. An in vitro stem cell study showed significant cell adhesion and proliferation over the fabricated HAp-COL and HAp-COL/HAp composite scaffolds. These results confirmed that fabrication of pure HAp with COL and COL/HAp materials had advanced effects on the mechanical properties of fabricated porous composite scaffolds.
DOI: 10.6084/m9.figshare.7992457.v2
title: Age-dependent accumulation of oligomeric SNCA/α-synuclein from impaired degradation in mutant LRRK2 knockin mouse model of Parkinson disease: role for therapeutic activation of chaperone-mediated autophagy (CMA)

description: Parkinson disease (PD) is an age-related neurodegenerative disorder associated with misfolded SNCA/α-synuclein accumulation in brain. Impaired catabolism of SNCA potentiates formation of its toxic oligomers. <i>LRRK2</i> (leucine-rich repeat kinase-2) mutations predispose to familial and sporadic PD. Mutant LRRK2 perturbs chaperone-mediated-autophagy (CMA) to degrade SNCA. We showed greater age-dependent accumulation of oligomeric SNCA in striatum and cortex of aged LRRK2<sup>R1441G</sup> knockin (KI) mice, compared to age-matched wildtype (WT) by 53% and 31%, respectively. Lysosomal clustering and accumulation of CMA-specific LAMP2A and HSPA8/HSC70 proteins were observed in aged mutant striatum along with increased GAPDH (CMA substrate) by immunohistochemistry of dorsal striatum and flow cytometry of ventral midbrain cells. Using our new reporter protein clearance assay, mutant mouse embryonic fibroblasts (MEFs) expressing either SNCA or CMA recognition ‘KFERQ’-like motif conjugated with photoactivated-PAmCherry showed slower cellular clearance compared to WT by 28% and 34%, respectively. However, such difference was not observed after the ‘KFERQ’-motif was mutated. LRRK2 mutant MEFs exhibited lower lysosomal degradation than WT indicating lysosomal dysfunction. LAMP2A-knockdown reduced total lysosomal activity and clearance of ‘KFERQ’-substrate in WT but not in mutant MEFs, indicating impaired CMA in the latter. A CMA-specific activator, AR7, induced neuronal LAMP2A transcription and lysosomal activity in MEFs. AR7 also attenuated the progressive accumulation of both intracellular and extracellular SNCA oligomers in prolonged cultures of mutant cortical neurons (DIV21), indicating that oligomer accumulation can be suppressed by CMA activation. Activation of autophagic pathways to reduce aged-related accumulation of pathogenic SNCA oligomers is a viable disease-modifying therapeutic strategy for PD. <b>Abbreviations:</b> 3-MA: 3-methyladenine; AR7: 7-chloro-3-(4-methylphenyl)-2H-1,4-benzoxazine; CMA: chaperone-mediated autophagy; CQ: chloroquine; CSF: cerebrospinal fluid; DDM: n-dodecyl β-D-maltoside; DIV: days in vitro; ELISA: enzyme-linked immunosorbent assay; FACS: fluorescence-activated cell sorting; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GWAS: genome-wide association studies; HSPA8/HSC70: heat shock protein 8; KFERQ: CMA recognition pentapeptide; KI: knockin; LAMP1: lysosomal-associated membrane protein 1; LAMP2A: lysosomal-associated membrane protein 2A; LDH: lactate dehydrogenase; LRRK2: leucine-rich repeat kinase 2; MEF: mouse embryonic fibroblast; NDUFS4: NADH:ubiquinone oxidoreductase core subunit S4; NE: novel epitope; PD: Parkinson disease; RARA/RARα: retinoic acid receptor, alpha; SNCA: synuclein, alpha; TUBB3/TUJ1: tubulin, beta 3 class III; WT: wild-type