cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1621397.v1
title: Benzoxazolinone Detoxification by <i>N</i>-Glucosylation: The Multi-Compartment- Network of <i>Zea mays</i> L

description: The major detoxification product in maize roots after 24h benzoxazolin-2(3<i>H</i>)-one (BOA) exposure was identified as glucoside carbamate resulting from rearrangement of BOA-<i>N</i>-glucoside, but the pathway of <i>N</i>-glucosylation, enzymes involved and the site of synthesis were previously unknown. Assaying whole cell proteins revealed the necessity of H<sub>2</sub>O<sub>2</sub> and Fe<sup>2</sup><sup>+</sup> ions for glucoside carbamate production. Peroxidase produced BOA radicals are apparently formed within the extraplastic space of the young maize root. Radicals seem to be the preferred substrate for <i>N</i>-glucosylation, either by direct reaction with glucose or, more likely, the <i>N</i>-glucoside is released by glucanase/glucosidase catalyzed hydrolysis from cell wall components harboring fixed BOA. The processes are accompanied by alterations of cell wall polymers. Glucoside carbamate accumulation could be suppressed by the oxireductase inhibitor 2-bromo-4´-nitroacetophenone and by peroxidase inhibitor 2,3-butanedione. Alternatively, activated BOA molecules with an open heterocycle may be produced by microorganisms (e.g., endophyte <i>Fusarium verticillioides</i>) and channeled for enzymatic <i>N</i>-glucosylation. Experiments with transgenic <i>Arabidopsis</i> lines indicate a role of maize glucosyltransferase BX9 in BOA-<i>N</i>-glycosylation. Western blots with BX9 antibody demonstrate the presence of BX9 in the extraplastic space. Proteomic analyses verified a high BOA responsiveness of multiple peroxidases in the apoplast/cell wall. BOA incubations led to shifting, altered abundances and identities of the apoplast and cell wall located peroxidases, glucanases, glucosidases and glutathione transferases (GSTs). GSTs could function as glucoside carbamate transporters. The highly complex, compartment spanning and redox-regulated glucoside carbamate pathway seems to be mainly realized in Poaceae. In maize, carbamate production is independent from benzoxazinone synthesis.
DOI: 10.6084/m9.figshare.1621389
title: Cell cycle-dependent changes in H3K56ac in human cells

description: The incorporation of histone H3 with an acetylated lysine 56 (H3K56ac) into the nucleosome is important for chromatin remodeling and serves as a marker of new nucleosomes during DNA replication and repair in yeast. However, in human cells, the level of H3K56ac is greatly reduced, and its role during the cell cycle is controversial. Our aim was to determine the potential of H3K56ac to regulate cell cycle progression in different human cell lines.A significant increase in the number of H3K56ac foci, but not in H3K56ac protein levels, was observed during the S and G2 phases in cancer but was not observed in embryonic stem cell lines. Despite this increase, the H3K56ac signal was not present in late replication chromatin, and H3K56ac protein levels did not decrease after the inhibition of DNA replication. H3K56ac was not tightly associated with the chromatin and was primarily localized to active chromatin regions. Our results support the role of H3K56ac in transcriptionally active chromatin areas but do not confirm H3K56ac as a marker of newly synthetized nucleosomes in DNA replication.
DOI: 10.6084/m9.figshare.1621384
title: Patient2_Tp7

description: DTI data at Time Point 7 of second MS patient
DOI: 10.6084/m9.figshare.1621385
title: Periconceptional folate consumption is associated with neonatal DNA methylation modifications in neural crest regulatory and cancer development genes

description: Folate deficiency during early embryonic development constitutes a risk factor for neural tube defects and potentially for childhood leukemia via unknown mechanisms. We tested whether folate consumption during the 12 months prior to conception induced DNA methylation modifications at birth in healthy neonates with a genome-wide and agnostic approach. We hypothesized that DNA methylation in genes involved in neural tube development and/or cancer susceptibility would be affected by folate exposure. We retrospectively assessed folate exposure at the time of conception by food-frequency questionnaires administered to the mothers of 347 healthy newborns. We measured genome-wide DNA methylation from neonatal blood spots. We implemented a method based on bootstrap resampling to decrease false-positive findings. Folate was inversely associated with DNA methylation throughout the genome. Among the top folate-associated genes that were replicated in an independent Gambian study were <i>TFAP2A</i>, a gene critical for neural crest development, <i>STX11</i>, a gene implicated in acute myeloid leukemia, and <i>CYS1</i>, a candidate gene for cystic kidney disease. Reduced periconceptional folate intake was associated with increased methylation and, in turn, decreased gene expression at these three loci. The top folate-sensitive genes defined by their associated CpG sites were enriched for numerous transcription factors by Gene Set Enrichment Analysis, including those implicated in cancer development (e.g., <i>MYC</i>-associated zinc finger protein). The influence of estimated periconceptional folate intake on neonatal DNA methylation levels provides potential mechanistic insights into the role of this vitamin in the development of neural tube defects and childhood cancers.
DOI: 10.6084/m9.figshare.1621389.v1
title: Cell cycle-dependent changes in H3K56ac in human cells

description: The incorporation of histone H3 with an acetylated lysine 56 (H3K56ac) into the nucleosome is important for chromatin remodeling and serves as a marker of new nucleosomes during DNA replication and repair in yeast. However, in human cells, the level of H3K56ac is greatly reduced, and its role during the cell cycle is controversial. Our aim was to determine the potential of H3K56ac to regulate cell cycle progression in different human cell lines.A significant increase in the number of H3K56ac foci, but not in H3K56ac protein levels, was observed during the S and G2 phases in cancer but was not observed in embryonic stem cell lines. Despite this increase, the H3K56ac signal was not present in late replication chromatin, and H3K56ac protein levels did not decrease after the inhibition of DNA replication. H3K56ac was not tightly associated with the chromatin and was primarily localized to active chromatin regions. Our results support the role of H3K56ac in transcriptionally active chromatin areas but do not confirm H3K56ac as a marker of newly synthetized nucleosomes in DNA replication.
DOI: 10.6084/m9.figshare.1621384.v1
title: Patient2_Tp7

description: DTI data at Time Point 7 of second MS patient
DOI: 10.6084/m9.figshare.1621385.v1
title: Periconceptional folate consumption is associated with neonatal DNA methylation modifications in neural crest regulatory and cancer development genes

description: Folate deficiency during early embryonic development constitutes a risk factor for neural tube defects and potentially for childhood leukemia via unknown mechanisms. We tested whether folate consumption during the 12 months prior to conception induced DNA methylation modifications at birth in healthy neonates with a genome-wide and agnostic approach. We hypothesized that DNA methylation in genes involved in neural tube development and/or cancer susceptibility would be affected by folate exposure. We retrospectively assessed folate exposure at the time of conception by food-frequency questionnaires administered to the mothers of 347 healthy newborns. We measured genome-wide DNA methylation from neonatal blood spots. We implemented a method based on bootstrap resampling to decrease false-positive findings. Folate was inversely associated with DNA methylation throughout the genome. Among the top folate-associated genes that were replicated in an independent Gambian study were <i>TFAP2A</i>, a gene critical for neural crest development, <i>STX11</i>, a gene implicated in acute myeloid leukemia, and <i>CYS1</i>, a candidate gene for cystic kidney disease. Reduced periconceptional folate intake was associated with increased methylation and, in turn, decreased gene expression at these three loci. The top folate-sensitive genes defined by their associated CpG sites were enriched for numerous transcription factors by Gene Set Enrichment Analysis, including those implicated in cancer development (e.g., <i>MYC</i>-associated zinc finger protein). The influence of estimated periconceptional folate intake on neonatal DNA methylation levels provides potential mechanistic insights into the role of this vitamin in the development of neural tube defects and childhood cancers.
DOI: 10.6084/m9.figshare.1621379
title: Patient2_Tp1

description: DTI data at Time Point 1 of second MS patient
DOI: 10.6084/m9.figshare.1621373
title: In <i>utero</i> arsenic exposure and epigenome-wide associations in placenta, umbilical artery, and human umbilical vein endothelial cells

description: Exposure to arsenic early in life has been associated with increased risk of several chronic diseases and is believed to alter epigenetic programming <i>in utero</i>. In the present study, we evaluate the epigenome-wide association of arsenic exposure <i>in utero</i> and DNA methylation in placenta (n = 37), umbilical artery (n = 45) and human umbilical vein endothelial cells (HUVEC) (n = 52) in a birth cohort using the Infinium HumanMethylation450 BeadChip array. Unadjusted and cell mixture adjusted associations for each tissue were examined along with enrichment analyses relative to CpG island location and omnibus permutation tests of association among biological pathways. One CpG in artery (cg26587014) and 4 CpGs in placenta (cg12825509; cg20554753; cg23439277; cg21055948) reached a Bonferroni adjusted level of significance. Several CpGs were differentially methylated in artery and placenta when controlling the false discovery rate (q-value&lt;0.05), but none in HUVEC. Enrichment of hypomethylated CpG islands was observed for artery while hypermethylation of open sea regions were present in placenta relative to prenatal arsenic exposure. The melanogenesis pathway was differentially methylated in artery (Max F <i>P</i> &lt; 0.001), placenta (Max F <i>P</i> &lt; 0.001), and HUVEC (Max F <i>P</i> = 0.02). Similarly, the insulin-signaling pathway was differentially methylated in artery (Max F <i>P</i> = 0.02), placenta (Max F <i>P</i> = 0.02), and HUVEC (Max F <i>P</i> = 0.02). Our results show that prenatal arsenic exposure can alter DNA methylation in artery and placenta but not in HUVEC. Further studies are needed to determine if these alterations in DNA methylation mediate the effect of prenatal arsenic exposure and health outcomes later in life.
DOI: 10.6084/m9.figshare.1621379.v1
title: Patient2_Tp1

description: DTI data at Time Point 1 of second MS patient
DOI: 10.6084/m9.figshare.1621372
title: A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers

description: Immortality is an essential characteristic of human carcinoma cells. We recently developed an efficient, reproducible method that immortalizes human mammary epithelial cells (HMEC) in the absence of gross genomic changes by targeting 2 critical senescence barriers. Consistent transcriptomic changes associated with immortality were identified using microarray analysis of isogenic normal finite pre-stasis, abnormal finite post-stasis, and immortal HMECs from 4 individuals. A total of 277 genes consistently changed in cells that transitioned from post-stasis to immortal. Gene ontology analysis of affected genes revealed biological processes significantly altered in the immortalization process. These immortalization-associated changes showed striking similarity to the gene expression changes seen in The Cancer Genome Atlas (TCGA) clinical breast cancer data. The most dramatic change in gene expression seen during the immortalization step was the downregulation of an unnamed, incompletely annotated transcript that we called <i>MORT</i>, for mortality, since its expression was closely associated with the mortal, finite lifespan phenotype. We show here that <i>MORT</i> (<i>ZNF667-AS1</i>) is expressed in all normal finite lifespan human cells examined to date and is lost in immortalized HMEC. <i>MORT</i> gene silencing at the mortal/immortal boundary was due to DNA hypermethylation of its CpG island promoter. This epigenetic silencing is also seen in human breast cancer cell lines and in a majority of human breast tumor tissues. The functional importance of DNA hypermethylation in <i>MORT</i> gene silencing is supported by the ability of 5-aza-2′-deoxycytidine to reactivate <i>MORT</i> expression. Analysis of TCGA data revealed deregulation of <i>MORT</i> expression due to DNA hypermethylation in 15 out of the 17 most common human cancers. The epigenetic silencing of <i>MORT</i> in a large majority of the common human cancers suggests a potential fundamental role in cellular immortalization during human carcinogenesis.
DOI: 10.6084/m9.figshare.1621373.v1
title: In <i>utero</i> arsenic exposure and epigenome-wide associations in placenta, umbilical artery, and human umbilical vein endothelial cells

description: Exposure to arsenic early in life has been associated with increased risk of several chronic diseases and is believed to alter epigenetic programming <i>in utero</i>. In the present study, we evaluate the epigenome-wide association of arsenic exposure <i>in utero</i> and DNA methylation in placenta (n = 37), umbilical artery (n = 45) and human umbilical vein endothelial cells (HUVEC) (n = 52) in a birth cohort using the Infinium HumanMethylation450 BeadChip array. Unadjusted and cell mixture adjusted associations for each tissue were examined along with enrichment analyses relative to CpG island location and omnibus permutation tests of association among biological pathways. One CpG in artery (cg26587014) and 4 CpGs in placenta (cg12825509; cg20554753; cg23439277; cg21055948) reached a Bonferroni adjusted level of significance. Several CpGs were differentially methylated in artery and placenta when controlling the false discovery rate (q-value&lt;0.05), but none in HUVEC. Enrichment of hypomethylated CpG islands was observed for artery while hypermethylation of open sea regions were present in placenta relative to prenatal arsenic exposure. The melanogenesis pathway was differentially methylated in artery (Max F <i>P</i> &lt; 0.001), placenta (Max F <i>P</i> &lt; 0.001), and HUVEC (Max F <i>P</i> = 0.02). Similarly, the insulin-signaling pathway was differentially methylated in artery (Max F <i>P</i> = 0.02), placenta (Max F <i>P</i> = 0.02), and HUVEC (Max F <i>P</i> = 0.02). Our results show that prenatal arsenic exposure can alter DNA methylation in artery and placenta but not in HUVEC. Further studies are needed to determine if these alterations in DNA methylation mediate the effect of prenatal arsenic exposure and health outcomes later in life.
DOI: 10.6084/m9.figshare.1621351
title: Patient1_Tp1

description: DTI data at Time Point 1 of first MS patient
DOI: 10.6084/m9.figshare.1621355
title: Patient1_Tp2

description: DTI data at Time Point 2 of first MS patient
DOI: 10.6084/m9.figshare.1621347.v1
title: Gaussian Job Archive for C19H23NaO7S

description: Archive of work produced using the resources of the Imperial College High Performance Computing Service.
DOI: 10.6084/m9.figshare.1621372.v1
title: A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers

description: Immortality is an essential characteristic of human carcinoma cells. We recently developed an efficient, reproducible method that immortalizes human mammary epithelial cells (HMEC) in the absence of gross genomic changes by targeting 2 critical senescence barriers. Consistent transcriptomic changes associated with immortality were identified using microarray analysis of isogenic normal finite pre-stasis, abnormal finite post-stasis, and immortal HMECs from 4 individuals. A total of 277 genes consistently changed in cells that transitioned from post-stasis to immortal. Gene ontology analysis of affected genes revealed biological processes significantly altered in the immortalization process. These immortalization-associated changes showed striking similarity to the gene expression changes seen in The Cancer Genome Atlas (TCGA) clinical breast cancer data. The most dramatic change in gene expression seen during the immortalization step was the downregulation of an unnamed, incompletely annotated transcript that we called <i>MORT</i>, for mortality, since its expression was closely associated with the mortal, finite lifespan phenotype. We show here that <i>MORT</i> (<i>ZNF667-AS1</i>) is expressed in all normal finite lifespan human cells examined to date and is lost in immortalized HMEC. <i>MORT</i> gene silencing at the mortal/immortal boundary was due to DNA hypermethylation of its CpG island promoter. This epigenetic silencing is also seen in human breast cancer cell lines and in a majority of human breast tumor tissues. The functional importance of DNA hypermethylation in <i>MORT</i> gene silencing is supported by the ability of 5-aza-2′-deoxycytidine to reactivate <i>MORT</i> expression. Analysis of TCGA data revealed deregulation of <i>MORT</i> expression due to DNA hypermethylation in 15 out of the 17 most common human cancers. The epigenetic silencing of <i>MORT</i> in a large majority of the common human cancers suggests a potential fundamental role in cellular immortalization during human carcinogenesis.
DOI: 10.6084/m9.figshare.1621351.v1
title: Patient1_Tp1

description: DTI data at Time Point 1 of first MS patient
DOI: 10.6084/m9.figshare.1621355.v1
title: Patient1_Tp2

description: DTI data at Time Point 2 of first MS patient
DOI: 10.6084/m9.figshare.1621318
title: Reducing bias in population and landscape genetic inferences: The effects of sampling related individuals and multiple life stages

description: Data and code used in the manuscript "Reducing bias in population and landscape genetic inferences: The effects of sampling related individuals and multiple life stages"
DOI: 10.6084/m9.figshare.1621305
title: TSP dataset

description: These data come from https://eden.dei.uc.pt/~paquete/tsp/.
DOI: 10.6084/m9.figshare.1621318.v2
title: Reducing bias in population and landscape genetic inferences: The effects of sampling related individuals and multiple life stages

description: Data and code used in the manuscript "Reducing bias in population and landscape genetic inferences: The effects of sampling related individuals and multiple life stages"
DOI: 10.6084/m9.figshare.1621318.v1
title: Reducing bias in population and landscape genetic inferences: The effects of sampling related individuals and multiple life stages

description: Data and code used in the manuscript "Reducing bias in population and landscape genetic inferences: The effects of sampling related individuals and multiple life stages"
DOI: 10.6084/m9.figshare.1621274
title: Incidence and risk factors of isolated systolic and diastolic hypertension: a 10 year follow-up of the Tehran Lipids and Glucose Study

description: The objective of this study is to examine the incidence and risk factors of isolated systolic hypertension (ISH) and isolated diastolic hypertension (IDH) in a Middle Eastern population, during a median follow-up of 9.6 years. In total, 8573 subjects without hypertension, cardiovascular disease and known diabetes were recruited into the study. To calculate the incidence of ISH, those with diastolic blood pressure (DBP) ≥ 90 mmHg during follow-up, and for calculating IDH those with systolic blood pressure (SBP) ≥ 140 mmHg during follow-up, were excluded. During follow-up, 235 new cases of ISH were identified, with a crude incidence rate of 5.7/1000 person-years; the corresponding values for IDH were 470 and 10.9/1000 person-years. Using backward stepwise Cox regression analysis, older age, baseline SBP and body mass index were related to incident ISH. Regarding IDH, younger age, baseline DBP and waist circumference were associated with higher risk, whereas female gender and being married were associated with lower risk (all <i>p</i>
DOI: 10.6084/m9.figshare.1621269
title: Dual-process of anthropomoprhism

description: Data from a study on dual-process of anthropomoprhism in Human-Robot Interaction
DOI: 10.6084/m9.figshare.1621274.v1
title: Incidence and risk factors of isolated systolic and diastolic hypertension: a 10 year follow-up of the Tehran Lipids and Glucose Study

description: The objective of this study is to examine the incidence and risk factors of isolated systolic hypertension (ISH) and isolated diastolic hypertension (IDH) in a Middle Eastern population, during a median follow-up of 9.6 years. In total, 8573 subjects without hypertension, cardiovascular disease and known diabetes were recruited into the study. To calculate the incidence of ISH, those with diastolic blood pressure (DBP) ≥ 90 mmHg during follow-up, and for calculating IDH those with systolic blood pressure (SBP) ≥ 140 mmHg during follow-up, were excluded. During follow-up, 235 new cases of ISH were identified, with a crude incidence rate of 5.7/1000 person-years; the corresponding values for IDH were 470 and 10.9/1000 person-years. Using backward stepwise Cox regression analysis, older age, baseline SBP and body mass index were related to incident ISH. Regarding IDH, younger age, baseline DBP and waist circumference were associated with higher risk, whereas female gender and being married were associated with lower risk (all <i>p</i>
DOI: 10.6084/m9.figshare.1621269.v1
title: Dual-process of anthropomoprhism

description: Data from a study on dual-process of anthropomoprhism in Human-Robot Interaction
DOI: 10.6084/m9.figshare.1621261
title: Analysis of Bibliometrics information for selecting the best field of study

description: Bibliometrics can be defined as the statistical analysis of publications. Bibliometrics has focused on the quantitative analysis of citations and citation counts which is complex. It is so complex and specialized that personal knowledge and experience are insufficient tools for understanding trends for making decisions. We need tools for analysis of Bibliometrics information for select the best field of study with promising enough attention. This presentation will provide tools to discover the new trends in our field of study in order to select an area for research and publication which promising the highest research impact.
DOI: 10.6084/m9.figshare.1621235
title: Effects of ABA and CaCl<sub>2</sub> on GABA accumulation in fava bean germinating under hypoxia-NaCl stress

description: Effects of exogenous abscisic acid (ABA) and CaCl<sub>2</sub> on γ-aminobutyric acid (GABA) accumulation of germinated fava bean under hypoxia-NaCl stress were investigated. Exogenous ABA resulted in the enhancement of glutamate decarboxylase (GAD) and diamine oxidase (DAO) activity as well as GABA content in cotyledon and shoot. CaCl<sub>2</sub> increased both enzyme activities in shoot and GABA content in cotyledon and shoot. ABA downregulated <i>GAD</i> expression in cotyledon and radicle, while upregulated that in shoot; it also upregulated <i>DAO</i> expression in each organ. CaCl<sub>2</sub> upregulated <i>GAD</i> expression in cotyledon, while downregulated that in radicle. However, it upregulated <i>DAO</i> expression in shoot, downregulated that in radicle. ABA inhibitor fluridon and ethylenediaminetetraacetic acid inhibited GAD and DAO activities significantly so that inhibited GABA accumulation through reducing ABA biosynthesis and chelating Ca<sup>2+</sup>, respectively. However, they upregulated <i>GAD</i> and <i>DAO</i> expression in varying degrees. These results indicate that ABA and Ca<sup>2+</sup> participate in GABA biosynthesis in fava bean during germination under hypoxia-NaCl stress.