cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1405694.v4
title: Modulation of insulin degrading enzyme activity and liver cell proliferation

description: Diabetes mellitus type 2 (T2DM), insulin therapy, and hyperinsulinemia are independent risk factors of liver cancer. Recently, the use of a novel inhibitor of insulin degrading enzyme (IDE) was proposed as a new therapeutic strategy in T2DM. However, IDE inhibition might stimulate liver cell proliferation via increased intracellular insulin concentration. The aim of this study was to characterize effects of inhibition of IDE activity in HepG2 hepatoma cells and to analyze liver specific expression of <i>IDE</i> in subjects with T2DM. HepG2 cells were treated with 10 nM insulin for 24 h with or without inhibition of IDE activity using <i>IDE</i> RNAi, and cell transcriptome and proliferation rate were analyzed. Human liver samples (n = 22) were used for the gene expression profiling by microarrays. In HepG2 cells, <i>IDE</i> knockdown changed expression of genes involved in cell cycle and apoptosis pathways. Proliferation rate was lower in <i>IDE</i> knockdown cells than in controls. Microarray analysis revealed the decrease of hepatic <i>IDE</i> expression in subjects with T2DM accompanied by the downregulation of the p53-dependent genes <i>FAS</i> and <i>CCNG2</i>, but not by the upregulation of proliferation markers <i>MKI67, MCM2</i> and <i>PCNA</i>. Similar results were found in the liver microarray dataset from GEO Profiles database. In conclusion, <i>IDE</i> expression is decreased in liver of subjects with T2DM which is accompanied by the dysregulation of p53 pathway. Prolonged use of IDE inhibitors for T2DM treatment should be carefully tested in animal studies regarding its potential effect on hepatic tumorigenesis.
DOI: 10.6084/m9.figshare.1405694.v3
title: Modulation of insulin degrading enzyme activity and liver cell proliferation

description: Diabetes mellitus type 2 (T2DM), insulin therapy, and hyperinsulinemia are independent risk factors of liver cancer. Recently, the use of a novel inhibitor of insulin degrading enzyme (IDE) was proposed as a new therapeutic strategy in T2DM. However, IDE inhibition might stimulate liver cell proliferation via increased intracellular insulin concentration. The aim of this study was to characterize effects of inhibition of IDE activity in HepG2 hepatoma cells and to analyze liver specific expression of <i>IDE</i> in subjects with T2DM. HepG2 cells were treated with 10 nM insulin for 24 h with or without inhibition of IDE activity using <i>IDE</i> RNAi, and cell transcriptome and proliferation rate were analyzed. Human liver samples (n = 22) were used for the gene expression profiling by microarrays. In HepG2 cells, <i>IDE</i> knockdown changed expression of genes involved in cell cycle and apoptosis pathways. Proliferation rate was lower in <i>IDE</i> knockdown cells than in controls. Microarray analysis revealed the decrease of hepatic <i>IDE</i> expression in subjects with T2DM accompanied by the downregulation of the p53-dependent genes <i>FAS</i> and <i>CCNG2</i>, but not by the upregulation of proliferation markers <i>MKI67, MCM2</i> and <i>PCNA</i>. Similar results were found in the liver microarray dataset from GEO Profiles database. In conclusion, <i>IDE</i> expression is decreased in liver of subjects with T2DM which is accompanied by the dysregulation of p53 pathway. Prolonged use of IDE inhibitors for T2DM treatment should be carefully tested in animal studies regarding its potential effect on hepatic tumorigenesis.
DOI: 10.6084/m9.figshare.1405701.v3
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.
DOI: 10.6084/m9.figshare.1406982.v7
title: The Recorder's Paradox

description: The need to access vernacular speech styles, which appear in informal, uncontrolled environments poses a problem for the recording of audio high enough in quality for acoustic analysis. As a result, sociolinguistic interviews are either relatively formal and controlled resulting in more formal speech and decent quality audio OR informal, uncontrolled contexts with a decent level of vernacular speech yet low quality audio. This poses a problem for the analysis of vernacular speech. Studies show the effects of noise on voice quality properties but are noisy environments actually detrimental to analysis of formant frequencies? Does noise affect all formants equally? What types of noise should be avoided?
DOI: 10.6084/m9.figshare.1405701.v4
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.
DOI: 10.6084/m9.figshare.1406982.v8
title: The Recorder's Paradox

description: The need to access vernacular speech styles, which appear in informal, uncontrolled environments poses a problem for the recording of audio high enough in quality for acoustic analysis. As a result, sociolinguistic interviews are either relatively formal and controlled resulting in more formal speech and decent quality audio OR informal, uncontrolled contexts with a decent level of vernacular speech yet low quality audio. This poses a problem for the analysis of vernacular speech. Studies show the effects of noise on voice quality properties but are noisy environments actually detrimental to analysis of formant frequencies? Does noise affect all formants equally? What types of noise should be avoided?
DOI: 10.6073/pasta/0d66d0ae643c6cfd14f64e6a60997b30
title: Nematode abundance in soil cores collected beneath mesquite trees in irrigated and non-irrigated plots at the Jornada Basin LTER site, 1988

description: This data package contains nematode abundance in soils subjected to an irrigation experiment in mesquite coppice dune habitats during the early years of Jornada Basin LTER (LTER-I and II). The purpose of this study was to quantify total nematode abundance, and the abundance of nematode functional groups, in irrigated and non-irrigated (control) soils beneath mesquite plants (Prosopis glandulosa). Soil cores were taken from three depths (0-50cm, 50-100cm, and 100-150cm) then divided into subsamples for nematode investigation. Nematodes were quantified via a semi-automatic elutriator with sugar flotation-sieving and the Baerman Funnel technique. Nematodes were counted and separated into trophic groups: fungal feeders, bacterial feeders, plant parasites, and omnivore-predators. The data collection began in March 1988 and ended in October 1988. This dataset is complete.
DOI: 10.6084/m9.figshare.1405701.v5
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.
DOI: 10.6084/m9.figshare.1406982.v10
title: The Recorder's Paradox: high fidelity from natural environments

description: The need to access vernacular speech styles, which appear in informal, uncontrolled environments poses a problem for the recording of audio high enough in quality for acoustic analysis. As a result, sociolinguistic interviews are either relatively formal and controlled resulting in more formal speech and decent quality audio OR informal, uncontrolled contexts with a decent level of vernacular speech yet low quality audio. This poses a problem for the analysis of vernacular speech. Studies show the effects of noise on voice quality properties but are noisy environments actually detrimental to analysis of formant frequencies? Does noise affect all formants equally? What types of noise should be avoided?
DOI: 10.6084/m9.figshare.1405701.v6
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.
DOI: 10.6084/m9.figshare.1406982.v9
title: The Recorder

description: The need to access vernacular speech styles, which appear in informal, uncontrolled environments poses a problem for the recording of audio high enough in quality for acoustic analysis. As a result, sociolinguistic interviews are either relatively formal and controlled resulting in more formal speech and decent quality audio OR informal, uncontrolled contexts with a decent level of vernacular speech yet low quality audio. This poses a problem for the analysis of vernacular speech. Studies show the effects of noise on voice quality properties but are noisy environments actually detrimental to analysis of formant frequencies? Does noise affect all formants equally? What types of noise should be avoided?
DOI: 10.6084/m9.figshare.1405701.v7
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.
DOI: 10.6084/m9.figshare.1405690.v1
title: Transcriptome profiling identifies p53 as a key player during calreticulin deficiency: Implications in lipid accumulation

description: Calreticulin (CRT) is an endoplasmic reticulum (ER) resident calcium binding protein that is involved in several cellular activities. Transcriptome analyses in CRT knockdown HepG2 cells revealed 253 altered unique genes and subsequent <i>in silico</i> protein-protein interaction network and MCODE clustering identified 34 significant clusters, of which p53 occupied the central hub node in the highest node-rich cluster. Towards validation, we show that CRT knockdown leads to inhibition of p53 protein levels. Both, CRT and p53 siRNA promote hepatic lipid accumulation and this was accompanied by elevated SREBP-1c and FAS levels. p53 was identified to bind at −219 bp on the SREBP-1c promoter and in the presence of CRT siRNA, there was decreased occupancy of p53 on this binding element. This was associated with increased SREBP-1c promoter activity and both, mutation in this binding site or p53 over-expression antagonised the effects of CRT knockdown. We, therefore, identify a negatively regulating p53 binding site on the SREBP-1c promoter that is critical during hepatic lipid accumulation. These results were validated in mouse primary hepatocytes and towards a physiological relevance, we report that while the levels of CRT and p53 are reduced in the fatty livers of diabetic db/db mice, SREBP-1c levels are significantly elevated. Our results suggest that decreased CRT levels might be involved in the development of a fatty liver by preventing p53 occupancy on the SREBP-1c promoter and thereby facilitating SREBP-1c up-regulation and consequently, lipid accumulation.
DOI: 10.6084/m9.figshare.1405701.v8
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.
DOI: 10.6084/m9.figshare.1405690.v2
title: Transcriptome profiling identifies p53 as a key player during calreticulin deficiency: Implications in lipid accumulation

description: Calreticulin (CRT) is an endoplasmic reticulum (ER) resident calcium binding protein that is involved in several cellular activities. Transcriptome analyses in CRT knockdown HepG2 cells revealed 253 altered unique genes and subsequent <i>in silico</i> protein-protein interaction network and MCODE clustering identified 34 significant clusters, of which p53 occupied the central hub node in the highest node-rich cluster. Toward validation, we show that CRT knockdown leads to inhibition of p53 protein levels. Both, CRT and p53 siRNA promote hepatic lipid accumulation and this was accompanied by elevated SREBP-1c and FAS levels. p53 was identified to bind at −219 bp on the SREBP-1c promoter and in the presence of CRT siRNA, there was decreased occupancy of p53 on this binding element. This was associated with increased SREBP-1c promoter activity and both, mutation in this binding site or p53 over-expression antagonised the effects of CRT knockdown. We, therefore, identify a negatively regulating p53 binding site on the SREBP-1c promoter that is critical during hepatic lipid accumulation. These results were validated in mouse primary hepatocytes and toward a physiological relevance, we report that while the levels of CRT and p53 are reduced in the fatty livers of diabetic db/db mice, SREBP-1c levels are significantly elevated. Our results suggest that decreased CRT levels might be involved in the development of a fatty liver by preventing p53 occupancy on the SREBP-1c promoter and thereby facilitating SREBP-1c up-regulation and consequently, lipid accumulation.
DOI: 10.6084/m9.figshare.1405701.v9
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.
DOI: 10.6084/m9.figshare.1405690
title: Transcriptome profiling identifies p53 as a key player during calreticulin deficiency: Implications in lipid accumulation

description: Calreticulin (CRT) is an endoplasmic reticulum (ER) resident calcium binding protein that is involved in several cellular activities. Transcriptome analyses in CRT knockdown HepG2 cells revealed 253 altered unique genes and subsequent <i>in silico</i> protein-protein interaction network and MCODE clustering identified 34 significant clusters, of which p53 occupied the central hub node in the highest node-rich cluster. Toward validation, we show that CRT knockdown leads to inhibition of p53 protein levels. Both, CRT and p53 siRNA promote hepatic lipid accumulation and this was accompanied by elevated SREBP-1c and FAS levels. p53 was identified to bind at −219 bp on the SREBP-1c promoter and in the presence of CRT siRNA, there was decreased occupancy of p53 on this binding element. This was associated with increased SREBP-1c promoter activity and both, mutation in this binding site or p53 over-expression antagonised the effects of CRT knockdown. We, therefore, identify a negatively regulating p53 binding site on the SREBP-1c promoter that is critical during hepatic lipid accumulation. These results were validated in mouse primary hepatocytes and toward a physiological relevance, we report that while the levels of CRT and p53 are reduced in the fatty livers of diabetic db/db mice, SREBP-1c levels are significantly elevated. Our results suggest that decreased CRT levels might be involved in the development of a fatty liver by preventing p53 occupancy on the SREBP-1c promoter and thereby facilitating SREBP-1c up-regulation and consequently, lipid accumulation.
DOI: 10.6084/m9.figshare.1405690.v4
title: Transcriptome profiling identifies p53 as a key player during calreticulin deficiency: Implications in lipid accumulation

description: Calreticulin (CRT) is an endoplasmic reticulum (ER) resident calcium binding protein that is involved in several cellular activities. Transcriptome analyses in CRT knockdown HepG2 cells revealed 253 altered unique genes and subsequent <i>in silico</i> protein-protein interaction network and MCODE clustering identified 34 significant clusters, of which p53 occupied the central hub node in the highest node-rich cluster. Toward validation, we show that CRT knockdown leads to inhibition of p53 protein levels. Both, CRT and p53 siRNA promote hepatic lipid accumulation and this was accompanied by elevated SREBP-1c and FAS levels. p53 was identified to bind at −219 bp on the SREBP-1c promoter and in the presence of CRT siRNA, there was decreased occupancy of p53 on this binding element. This was associated with increased SREBP-1c promoter activity and both, mutation in this binding site or p53 over-expression antagonised the effects of CRT knockdown. We, therefore, identify a negatively regulating p53 binding site on the SREBP-1c promoter that is critical during hepatic lipid accumulation. These results were validated in mouse primary hepatocytes and toward a physiological relevance, we report that while the levels of CRT and p53 are reduced in the fatty livers of diabetic db/db mice, SREBP-1c levels are significantly elevated. Our results suggest that decreased CRT levels might be involved in the development of a fatty liver by preventing p53 occupancy on the SREBP-1c promoter and thereby facilitating SREBP-1c up-regulation and consequently, lipid accumulation.
DOI: 10.6084/m9.figshare.1405701.v10
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.
DOI: 10.6084/m9.figshare.1405690.v3
title: Transcriptome profiling identifies p53 as a key player during calreticulin deficiency: Implications in lipid accumulation

description: Calreticulin (CRT) is an endoplasmic reticulum (ER) resident calcium binding protein that is involved in several cellular activities. Transcriptome analyses in CRT knockdown HepG2 cells revealed 253 altered unique genes and subsequent <i>in silico</i> protein-protein interaction network and MCODE clustering identified 34 significant clusters, of which p53 occupied the central hub node in the highest node-rich cluster. Toward validation, we show that CRT knockdown leads to inhibition of p53 protein levels. Both, CRT and p53 siRNA promote hepatic lipid accumulation and this was accompanied by elevated SREBP-1c and FAS levels. p53 was identified to bind at −219 bp on the SREBP-1c promoter and in the presence of CRT siRNA, there was decreased occupancy of p53 on this binding element. This was associated with increased SREBP-1c promoter activity and both, mutation in this binding site or p53 over-expression antagonised the effects of CRT knockdown. We, therefore, identify a negatively regulating p53 binding site on the SREBP-1c promoter that is critical during hepatic lipid accumulation. These results were validated in mouse primary hepatocytes and toward a physiological relevance, we report that while the levels of CRT and p53 are reduced in the fatty livers of diabetic db/db mice, SREBP-1c levels are significantly elevated. Our results suggest that decreased CRT levels might be involved in the development of a fatty liver by preventing p53 occupancy on the SREBP-1c promoter and thereby facilitating SREBP-1c up-regulation and consequently, lipid accumulation.
DOI: 10.6084/m9.figshare.1405689.v1
title: Heterogeneous cell-cycle behavior in response to UVB irradiation by a population of single cancer cells visualized by time-lapse FUCCI imaging

description: The present study analyzed the heterogeneous cell-cycle dependence and fate of single cancer cells in a population treated with UVB using a fluorescence ubiquitination-based cell-cycle (FUCCI) imaging system. HeLa cells expressing FUCCI were irradiated by 100 or 200 J/m<sup>2</sup> UVB. Modulation of the cell-cycle and apoptosis were observed by time-lapse confocal microscopy imaging every 30 min for 72 h. Correlation between cell survival and factors including cell-cycle phase at the time of the irradiation of UVB, mitosis and the G<sub>1</sub>/S transition were analyzed using the Kaplan–Meier method along with the log rank test. Time-lapse FUCCI imaging of HeLa cells demonstrated that UVB irradiation induced cell-cycle arrest in S/G<sub>2</sub>/M phase in the majority of the cells. The cells irradiated by 100 or 200 J/m<sup>2</sup> UVB during G<sub>0</sub>/G<sub>1</sub> phase had a higher survival rate than the cells irradiated during S/G<sub>2</sub>/M phase. A minority of cells could escape S/G<sub>2</sub>/M arrest and undergo mitosis which significantly correlated with decreased survival of the cells. In contrast, G<sub>1</sub>/S transition significantly correlated with increased survival of the cells after UVB irradiation. UVB at 200 J/m<sup>2</sup> resulted in a greater number of apoptotic cells.
DOI: 10.6084/m9.figshare.1405687
title: DEK over-expression promotes mitotic defects and micronucleus formation

description: The <i>DEK</i> gene encodes a nuclear protein that binds chromatin and is involved in various fundamental nuclear processes including transcription, RNA splicing, DNA replication and DNA repair. Several cancer types characteristically over-express DEK at the earliest stages of transformation. In order to explore relevant mechanisms whereby DEK supports oncogenicity, we utilized cancer databases to identify gene transcripts whose expression patterns are tightly correlated with that of DEK. We identified an enrichment of genes involved in mitosis and thus investigated the regulation and possible function of DEK in cell division. Immunofluorescence analyses revealed that DEK dissociates from DNA in early prophase and re-associates with DNA during telophase in human keratinocytes. Mitotic cell populations displayed a sharp reduction in DEK protein levels compared to the corresponding interphase population, suggesting DEK may be degraded or otherwise removed from the cell prior to mitosis. Interestingly, DEK overexpression stimulated its own aberrant association with chromatin throughout mitosis. Furthermore, DEK co-localized with anaphase bridges, chromosome fragments, and micronuclei, suggesting a specific association with mitotically defective chromosomes. We found that DEK over-expression in both non-transformed and transformed cells is sufficient to stimulate micronucleus formation. These data support a model wherein normal chromosomal clearance of DEK is required for maintenance of high fidelity cell division and chromosomal integrity. Therefore, the overexpression of DEK and its incomplete removal from mitotic chromosomes promotes genomic instability through the generation of genetically abnormal daughter cells. Consequently, DEK over-expression may be involved in the initial steps of developing oncogenic mutations in cells leading to cancer initiation
DOI: 10.6084/m9.figshare.1405701.v11
title: Cuke Particle Positions - 1998-2007 - Grid sites

description: LTRANS V2 raw output: Longitude, Latitude, depth, boundary status, and release site. Directories are structured as G1998\152\1\ meaning treatmentyear\releaseday\bin\. Files are named para 1002.csv which contains all the positions (of that treatment, year, site, and release day) at the end of the first day.