cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1285531.v2
title: Social context of the Old Kingdom copper model tools

description: Copper model tools were usually part of the elite burial equipment during the Old Kingdom in the Ancient Egypt. Definition of tool types is based on the semiotic triangle and a correct reading and interpretation of the artefacts is approached here. Model tools present in the burial equipment were tools for stone- and wood-working, these being materials of conspicuous consumption in the period. Tools are examined as symbols of the patron–craftsman relationship, where the ownership of the copper tools was the patron’s. Copper model tools were standardized and a connection between the size and amount of copper model tools and social status of the buried persons is explored. Persons with higher status had access to larger amounts of copper; however, the rules of the access were changing and access to copper was widening during the Old Kingdom.
DOI: 10.6084/m9.figshare.1285531.v1
title: Social context of the Old Kingdom copper model tools

description: Copper model tools were usually part of the elite burial equipment during the Old Kingdom in the Ancient Egypt. Definition of tool types is based on the semiotic triangle and a correct reading and interpretation of the artefacts is approached here. Model tools present in the burial equipment were tools for stone- and wood-working, these being materials of conspicuous consumption in the period. Tools are examined as symbols of the patron–craftsman relationship, where the ownership of the copper tools was the patron’s. Copper model tools were standardized and a connection between the size and amount of copper model tools and social status of the buried persons is explored. Persons with higher status had access to larger amounts of copper; however, the rules of the access were changing and access to copper was widening during the Old Kingdom.
DOI: 10.6084/m9.figshare.1285524
title: Ethanol’s growing demand and belowground biodiversity: soil macroinvertebrate community responses to sugarcane expansion in Brazil

description: We examined the soil macrofaunal community responses to sugarcane (Saccharum spp.) expansion from pasturelands, and the relationship to the contents and plant availability of soil phosphorus, the main agriculture-limiting nutrient in tropical soils. We sampled 3 field sites to represent the Brazilian sugarcane-expansion region. In each field site we identified one chronosequence comprising a 30 years old conversion from native vegetation to pasture , and a conversion from PA to sugarcane differing in time between the 3 field sites.
DOI: 10.6084/m9.figshare.1285523
title: Differential regulation of MCM7 and its intronic miRNA cluster miR-106b-25 during megakaryopoiesis induced polyploidy

description: Megakaryocytes exit from mitotic cell cycle and enter a phase of repeated DNA replication without undergoing cell division, in a process termed as endomitosis of which little is known. We studied the expression of a DNA replication licensing factor mini chromosome maintenance protein 7 (MCM7) and its intronic miR-106b-25 cluster during mitotic and endo-mitotic cycles in megakaryocytic cell lines and <i>in vitro</i> cultured megakaryocytes obtained from human cord blood derived CD34<sup>+</sup> cells. Our results show that contrary to mitotic cell cycle, endomitosis proceeds with an un-coupling of the expression of MCM7 and miR-106b-25. This was attributed to the presence of a transcript variant of MCM7 which undergoes nonsense mediated decay (NMD). Additionally, miR-25 which was up regulated during endomitosis was found to promote megakaryopoiesis by inhibiting the expression of PTEN. Our study thus highlights the importance of a transcript variant of MCM7 destined for NMD in the modulation of megakaryopoiesis.
DOI: 10.6084/m9.figshare.1285524.v1
title: Ethanol’s growing demand and belowground biodiversity: soil macroinvertebrate community responses to sugarcane expansion in Brazil

description: We examined the soil macrofaunal community responses to sugarcane (Saccharum spp.) expansion from pasturelands, and the relationship to the contents and plant availability of soil phosphorus, the main agriculture-limiting nutrient in tropical soils. We sampled 3 field sites to represent the Brazilian sugarcane-expansion region. In each field site we identified one chronosequence comprising a 30 years old conversion from native vegetation to pasture , and a conversion from PA to sugarcane differing in time between the 3 field sites.
DOI: 10.6084/m9.figshare.1285523.v1
title: Differential regulation of MCM7 and its intronic miRNA cluster miR-106b-25 during megakaryopoiesis induced polyploidy

description: SUMMARYMegakaryocytes exit from mitotic cell cycle and enter a phase of repeated DNA replication without undergoing cell division, in a process termed as endomitosis of which little is known. We studied the expression of a DNA replication licensing factor mini chromosome maintenance protein 7 (MCM7) and its intronic miR-106b-25 cluster during mitotic and endo-mitotic cycles in megakaryocytic cell lines and <i>in vitro</i> cultured megakaryocytes obtained from human cord blood derived CD34<sup>+</sup> cells. Our results show that contrary to mitotic cell cycle, endomitosis proceeds with an un-coupling of the expression of MCM7 and miR-106b-25. This was attributed to the presence of a transcript variant of MCM7 which undergoes nonsense mediated decay (NMD). Additionally, miR-25 which was up regulated during endomitosis was found to promote megakaryopoiesis by inhibiting the expression of PTEN. Our study thus highlights the importance of a transcript variant of MCM7 destined for NMD in the modulation of megakaryopoiesis.
DOI: 10.6084/m9.figshare.1285521.v1
title: MicroRNA-215 Regulates Fibroblast Function: Insights from a Human Fibrotic Disease

description: ABSTRACTMicroRNAs are implicated in the regulation of gene expression via various mechanisms in health and disease, including fibrotic processes. Pterygium is an ocular surface condition characterized by abnormal fibroblast proliferation and matrix deposition. We aimed to investigate the role of microRNAs in pterygium and understand the relevant cellular and molecular mechanisms. To achieve this objective, a combination of approaches using surgically excised paired human pterygium and conjunctival tissues as well as cultured primary fibroblast cells from tissue explants were evaluated. Fibroblast dysfunction has been shown to play a central role in pterygium pathology.Here we show that MiR-215, among a few others, was down-regulated (2 fold) in pterygium compared to control, and this was consistent in microarray, real-time PCR and fluorescent <i>in-situ</i> hybridization. The effects of increased miR-215 were investigated by adding exogenous miR-215 to fibroblasts, and this showed a decrease in cell proliferation but no significant apoptosis compared to control. Further cell cycle analysis showed that miR-215 depressed progression of cells at G1/S as well as G2/M. A few cell cycle related transcripts were down-regulated (2.2-4.5 fold) on addition of miR-215: Mcm3, Dicer1, Cdc25A, Ick, Trip13 and Mcm10. Theoretic binding energies were used to predict miR-215 binding targets and luciferase reporter studies confirmed Mcm10 and Cdc25A as direct targets.In summary, mir-215 could play a role in inhibiting fibroblast proliferation in ocular surface conjunctiva. Dampening of this mir-215 could result in increased fibroblast cell cycling and proliferation, with possibly increased fibroblastic production of matrix, inducing pterygium formation.
DOI: 10.6084/m9.figshare.1285523.v2
title: Differential regulation of MCM7 and its intronic miRNA cluster miR-106b-25 during megakaryopoiesis induced polyploidy

description: Megakaryocytes exit from mitotic cell cycle and enter a phase of repeated DNA replication without undergoing cell division, in a process termed as endomitosis of which little is known. We studied the expression of a DNA replication licensing factor mini chromosome maintenance protein 7 (MCM7) and its intronic miR-106b-25 cluster during mitotic and endo-mitotic cycles in megakaryocytic cell lines and <i>in vitro</i> cultured megakaryocytes obtained from human cord blood derived CD34<sup>+</sup> cells. Our results show that contrary to mitotic cell cycle, endomitosis proceeds with an un-coupling of the expression of MCM7 and miR-106b-25. This was attributed to the presence of a transcript variant of MCM7 which undergoes nonsense mediated decay (NMD). Additionally, miR-25 which was up regulated during endomitosis was found to promote megakaryopoiesis by inhibiting the expression of PTEN. Our study thus highlights the importance of a transcript variant of MCM7 destined for NMD in the modulation of megakaryopoiesis.
DOI: 10.6084/m9.figshare.1285523.v4
title: Differential regulation of MCM7 and its intronic miRNA cluster miR-106b-25 during megakaryopoiesis induced polyploidy

description: Megakaryocytes exit from mitotic cell cycle and enter a phase of repeated DNA replication without undergoing cell division, in a process termed as endomitosis of which little is known. We studied the expression of a DNA replication licensing factor mini chromosome maintenance protein 7 (MCM7) and its intronic miR-106b-25 cluster during mitotic and endo-mitotic cycles in megakaryocytic cell lines and <i>in vitro</i> cultured megakaryocytes obtained from human cord blood derived CD34<sup>+</sup> cells. Our results show that contrary to mitotic cell cycle, endomitosis proceeds with an un-coupling of the expression of MCM7 and miR-106b-25. This was attributed to the presence of a transcript variant of MCM7 which undergoes nonsense mediated decay (NMD). Additionally, miR-25 which was up regulated during endomitosis was found to promote megakaryopoiesis by inhibiting the expression of PTEN. Our study thus highlights the importance of a transcript variant of MCM7 destined for NMD in the modulation of megakaryopoiesis.
DOI: 10.6084/m9.figshare.1285521.v2
title: MicroRNA-215 Regulates Fibroblast Function: Insights from a Human Fibrotic Disease

description: MicroRNAs are implicated in the regulation of gene expression via various mechanisms in health and disease, including fibrotic processes. Pterygium is an ocular surface condition characterized by abnormal fibroblast proliferation and matrix deposition. We aimed to investigate the role of microRNAs in pterygium and understand the relevant cellular and molecular mechanisms. To achieve this objective, a combination of approaches using surgically excised paired human pterygium and conjunctival tissues as well as cultured primary fibroblast cells from tissue explants were evaluated. Fibroblast dysfunction has been shown to play a central role in pterygium pathology. Here we show that miR-215, among a few others, was down-regulated (2-fold) in pterygium compared to control, and this was consistent in microarray, real-time PCR and fluorescent <i>in-situ</i> hybridization. The effects of increased miR-215 were investigated by adding exogenous miR-215 to fibroblasts, and this showed a decrease in cell proliferation but no significant apoptosis compared to control. Further cell cycle analysis showed that miR-215 depressed progression of cells at G1/S as well as G2/M. A few cell cycle related transcripts were downregulated (2.2–4.5-fold) on addition of miR-215: Mcm3, Dicer1, Cdc25A, Ick, Trip13 and Mcm10. Theoretic binding energies were used to predict miR-215 binding targets and luciferase reporter studies confirmed Mcm10 and Cdc25A as direct targets. In summary, mir-215 could play a role in inhibiting fibroblast proliferation in ocular surface conjunctiva. Dampening of this mir-215 could result in increased fibroblast cell cycling and proliferation, with possibly increased fibroblastic production of matrix, inducing pterygium formation.
DOI: 10.6084/m9.figshare.1285523.v3
title: Differential regulation of MCM7 and its intronic miRNA cluster miR-106b-25 during megakaryopoiesis induced polyploidy

description: Megakaryocytes exit from mitotic cell cycle and enter a phase of repeated DNA replication without undergoing cell division, in a process termed as endomitosis of which little is known. We studied the expression of a DNA replication licensing factor mini chromosome maintenance protein 7 (MCM7) and its intronic miR-106b-25 cluster during mitotic and endo-mitotic cycles in megakaryocytic cell lines and <i>in vitro</i> cultured megakaryocytes obtained from human cord blood derived CD34<sup>+</sup> cells. Our results show that contrary to mitotic cell cycle, endomitosis proceeds with an un-coupling of the expression of MCM7 and miR-106b-25. This was attributed to the presence of a transcript variant of MCM7 which undergoes nonsense mediated decay (NMD). Additionally, miR-25 which was up regulated during endomitosis was found to promote megakaryopoiesis by inhibiting the expression of PTEN. Our study thus highlights the importance of a transcript variant of MCM7 destined for NMD in the modulation of megakaryopoiesis.
DOI: 10.6084/m9.figshare.1285521.v3
title: MicroRNA-215 Regulates Fibroblast Function: Insights from a Human Fibrotic Disease

description: MicroRNAs are implicated in the regulation of gene expression via various mechanisms in health and disease, including fibrotic processes. Pterygium is an ocular surface condition characterized by abnormal fibroblast proliferation and matrix deposition. We aimed to investigate the role of microRNAs in pterygium and understand the relevant cellular and molecular mechanisms. To achieve this objective, a combination of approaches using surgically excised paired human pterygium and conjunctival tissues as well as cultured primary fibroblast cells from tissue explants were evaluated. Fibroblast dysfunction has been shown to play a central role in pterygium pathology. Here we show that miR-215, among a few others, was down-regulated (2-fold) in pterygium compared to control, and this was consistent in microarray, real-time PCR and fluorescent <i>in-situ</i> hybridization. The effects of increased miR-215 were investigated by adding exogenous miR-215 to fibroblasts, and this showed a decrease in cell proliferation but no significant apoptosis compared to control. Further cell cycle analysis showed that miR-215 depressed progression of cells at G1/S as well as G2/M. A few cell cycle related transcripts were downregulated (2.2–4.5-fold) on addition of miR-215: Mcm3, Dicer1, Cdc25A, Ick, Trip13 and Mcm10. Theoretic binding energies were used to predict miR-215 binding targets and luciferase reporter studies confirmed Mcm10 and Cdc25A as direct targets. In summary, mir-215 could play a role in inhibiting fibroblast proliferation in ocular surface conjunctiva. Dampening of this mir-215 could result in increased fibroblast cell cycling and proliferation, with possibly increased fibroblastic production of matrix, inducing pterygium formation.
DOI: 10.6084/m9.figshare.1285515
title: Sizing the Problem of Improving Discovery and Access to NIH-funded Data: A preliminary study

description: To inform efforts to improve the discoverability of and access to biomedical datasets by providing a preliminary estimate of the number and type of datasets generated annually by National Institutes of Health (NIH)-funded researchers. Of particular interest is characterizing those datasets that are not deposited in a known data repository or registry, e.g., those for which a related journal article does not indicate that underlying data have been deposited in a known repository. Such “invisible” datasets comprise the “long tail” of biomedical data and pose significant practical challenges to ongoing efforts to improve discoverability of and access to biomedical research data. This study identified datasets used to support the NIH-funded research reported in articles published in 2011 and cited in PubMed® and deposited in PubMed Central® (PMC). After searching for all articles that acknowledged NIH support, we first identified articles that contained explicit mention of datasets being deposited in recognized repositories. Thirty members of the NIH staff then analyzed a random sample of the remaining articles to estimate how many and what types of datasets were used per article. Two reviewers independently examined each paper. Each dataset is titled <strong>Bigdata_randomsample_xxxx_xx</strong>. The <strong>xxxx</strong> refers to the set of articles the annotator looked at, while the <strong>xx</strong>identifies the annotator that did the analysis. Within each dataset, the author has listed the number of datasets they identified within the articles that they looked at. For every dataset that was found, the annotators were asked to insert a new row into the spreadsheet, and then describe the dataset they found (e.g., type of data, subject of study, etc.). Each row in the spreadsheet was always prepended by the PubMed Identifier (PMID) where the dataset was found. Finally, the files<strong> 2013-08-07_Bigdatastudy_dataanalysis, </strong><strong>Dataanalysis_ack_si_datasets</strong>, and <strong>Datasets additional random sample mention vs deposit 20150313 </strong>refer to the analysis that was performed based on each annotator's analysis of the publications they were assigned, and the data deposits identified from the analysis.
DOI: 10.6084/m9.figshare.1285521
title: MicroRNA-215 Regulates Fibroblast Function: Insights from a Human Fibrotic Disease

description: MicroRNAs are implicated in the regulation of gene expression via various mechanisms in health and disease, including fibrotic processes. Pterygium is an ocular surface condition characterized by abnormal fibroblast proliferation and matrix deposition. We aimed to investigate the role of microRNAs in pterygium and understand the relevant cellular and molecular mechanisms. To achieve this objective, a combination of approaches using surgically excised paired human pterygium and conjunctival tissues as well as cultured primary fibroblast cells from tissue explants were evaluated. Fibroblast dysfunction has been shown to play a central role in pterygium pathology. Here we show that miR-215, among a few others, was down-regulated (2-fold) in pterygium compared to control, and this was consistent in microarray, real-time PCR and fluorescent <i>in-situ</i> hybridization. The effects of increased miR-215 were investigated by adding exogenous miR-215 to fibroblasts, and this showed a decrease in cell proliferation but no significant apoptosis compared to control. Further cell cycle analysis showed that miR-215 depressed progression of cells at G1/S as well as G2/M. A few cell cycle related transcripts were downregulated (2.2–4.5-fold) on addition of miR-215: Mcm3, Dicer1, Cdc25A, Ick, Trip13 and Mcm10. Theoretic binding energies were used to predict miR-215 binding targets and luciferase reporter studies confirmed Mcm10 and Cdc25A as direct targets. In summary, mir-215 could play a role in inhibiting fibroblast proliferation in ocular surface conjunctiva. Dampening of this mir-215 could result in increased fibroblast cell cycling and proliferation, with possibly increased fibroblastic production of matrix, inducing pterygium formation.
DOI: 10.6084/m9.figshare.1285521.v5
title: MicroRNA-215 Regulates Fibroblast Function: Insights from a Human Fibrotic Disease

description: MicroRNAs are implicated in the regulation of gene expression via various mechanisms in health and disease, including fibrotic processes. Pterygium is an ocular surface condition characterized by abnormal fibroblast proliferation and matrix deposition. We aimed to investigate the role of microRNAs in pterygium and understand the relevant cellular and molecular mechanisms. To achieve this objective, a combination of approaches using surgically excised paired human pterygium and conjunctival tissues as well as cultured primary fibroblast cells from tissue explants were evaluated. Fibroblast dysfunction has been shown to play a central role in pterygium pathology. Here we show that miR-215, among a few others, was down-regulated (2-fold) in pterygium compared to control, and this was consistent in microarray, real-time PCR and fluorescent <i>in-situ</i> hybridization. The effects of increased miR-215 were investigated by adding exogenous miR-215 to fibroblasts, and this showed a decrease in cell proliferation but no significant apoptosis compared to control. Further cell cycle analysis showed that miR-215 depressed progression of cells at G1/S as well as G2/M. A few cell cycle related transcripts were downregulated (2.2–4.5-fold) on addition of miR-215: Mcm3, Dicer1, Cdc25A, Ick, Trip13 and Mcm10. Theoretic binding energies were used to predict miR-215 binding targets and luciferase reporter studies confirmed Mcm10 and Cdc25A as direct targets. In summary, mir-215 could play a role in inhibiting fibroblast proliferation in ocular surface conjunctiva. Dampening of this mir-215 could result in increased fibroblast cell cycling and proliferation, with possibly increased fibroblastic production of matrix, inducing pterygium formation.
DOI: 10.6084/m9.figshare.1285521.v4
title: MicroRNA-215 Regulates Fibroblast Function: Insights from a Human Fibrotic Disease

description: MicroRNAs are implicated in the regulation of gene expression via various mechanisms in health and disease, including fibrotic processes. Pterygium is an ocular surface condition characterized by abnormal fibroblast proliferation and matrix deposition. We aimed to investigate the role of microRNAs in pterygium and understand the relevant cellular and molecular mechanisms. To achieve this objective, a combination of approaches using surgically excised paired human pterygium and conjunctival tissues as well as cultured primary fibroblast cells from tissue explants were evaluated. Fibroblast dysfunction has been shown to play a central role in pterygium pathology. Here we show that miR-215, among a few others, was down-regulated (2-fold) in pterygium compared to control, and this was consistent in microarray, real-time PCR and fluorescent <i>in-situ</i> hybridization. The effects of increased miR-215 were investigated by adding exogenous miR-215 to fibroblasts, and this showed a decrease in cell proliferation but no significant apoptosis compared to control. Further cell cycle analysis showed that miR-215 depressed progression of cells at G1/S as well as G2/M. A few cell cycle related transcripts were downregulated (2.2–4.5-fold) on addition of miR-215: Mcm3, Dicer1, Cdc25A, Ick, Trip13 and Mcm10. Theoretic binding energies were used to predict miR-215 binding targets and luciferase reporter studies confirmed Mcm10 and Cdc25A as direct targets. In summary, mir-215 could play a role in inhibiting fibroblast proliferation in ocular surface conjunctiva. Dampening of this mir-215 could result in increased fibroblast cell cycling and proliferation, with possibly increased fibroblastic production of matrix, inducing pterygium formation.
DOI: 10.6084/m9.figshare.1285459
title: Dataset for "A cohort study of morbidity, mortality and health seeking behavior following rural health center visits by children under 12 in Southwestern Uganda"

description: Data used in the publication of the manuscript entitled "A cohort study of morbidity, mortality and health seeking behavior following rural health center visits by children under 12 in Southwestern Uganda" published in PLOS ONE
DOI: 10.6084/m9.figshare.1285424
title: Data from Rapidly increasing methyl mercury in endangered Ivory Gull (Pagophila eburnea) feathers over a 130-year record

description: Specimen collection data, stable isotope values (δ13C, δ15N), total and methyl mercury concentrations, and museum catalogue numbers. Data to accompany Bond, AL, Hobson, KA, and Branfireun, BA. 2015 Rapidly increasing methyl mercury in endangered Ivory Gull (<em>Pagophila eburnea</em>) feathers over a 130-year record. Proceedings of the Royal Society of London B Biological Sciences 282: 20150032