cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1255031.v1
title: Syntheses, Characterization, and Crystal Structures of Bromido-Coordinated Zinc(II) Complexes With Multidentate Schiff Bases

description: A new dinuclear bromido-coordinated Schiff base zinc(II) complex, [Zn<sub>2</sub>Br<sub>2</sub>L<sup>1</sup>(MeOH)]·MeOH (1), and a new mononuclear bromido-coordinated Schiff base zinc(II) complex, [ZnBr<sub>2</sub>L<sup>2</sup>] (2), where L<sup>1</sup> is the dianionic form of <i>N,N’</i>-bis(5-fluoro-2-hydroxybenzylidene)propane-1,3-diamine (H<sub>2</sub>L<sup>1</sup>), and L<sup>2</sup> is the zwitterionic form of 2-[(3-dimethylammoniopropylimino)methyl]-4-fluorophenol, have been preprared and characterized mainly by single-crystal X-ray diffraction. Complex 1 crystallizes in the monoclinic space group <i>P</i>2<sub>1</sub>/<i>n</i> with unit cell dimensions <i>a</i> = 10.0876(9) Å, <i>b</i> = 8.9549(8) Å, <i>c</i> = 26.586(2) Å, β = 95.134(2)º, V = 2391.9(4) Ǻ<sup>3</sup>, Z = 4, <i>R</i><sub>1</sub> = 0.0547, and <i>wR</i><sub>2</sub> = 0.1025. Complex 2 crystallizes in the monoclinic space group <i>P</i>2<sub>1</sub>/<i>c</i> with unit cell dimensions <i>a</i> = 7.359(1) Å, <i>b</i> = 13.798(2) Å, <i>c</i> = 17.676(2) Å, β = 114.602(2)º, V = 1631.8(4) Ǻ<sup>3</sup>, Z = 4, <i>R</i><sub>1</sub> = 0.0877, and <i>wR</i><sub>2</sub> = 0.2197. The inner Zn atom in 1 is five-coordinated in a square pyramidal geometry. The outer Zn atom in 1 and the Zn atom in 2 are four-coordinated in tetrahedral geometry. The crystals of the complexes are stabilized by intermolecular hydrogen bonds.
DOI: 10.6084/m9.figshare.1255042.v1
title: Supplement material

description: Supplement material for: Kraus, A. A. & Scholderer, J. (conditional accepted). Indirect measurement of motivation: Developing and testing a motivational Recoding-Free Implicit Association Test (m-IAT-RF).
DOI: 10.6084/m9.figshare.1255043.v1
title: ClinicalTrials.gov (Search Date: Dec 1st, 2014) = 3712 studies: Closed Studies | Interventional Studies | cancer | Phase 3

description: This database complies with the terms and conditions of ClinicalTrials.gov. Preliminary analysis will be disclosed soon via fig<strong>share.</strong>
DOI: 10.6084/m9.figshare.1255042.v2
title: Supplement material for "Kraus, A. A. & Scholderer, J. (conditionally accepted). Indirect measurement of motivation: Developing and testing a motivational Recoding-Free Implicit Association Test (m-IAT-RF)."

description: Supplement material for: Kraus, A. A. & Scholderer, J. (conditional accepted). Indirect measurement of motivation: Developing and testing a motivational Recoding-Free Implicit Association Test (m-IAT-RF).
DOI: 10.6084/m9.figshare.1255056.v2
title: Validation of the Bipolar Disorder Etiology Scale based on Psychological Behaviorism Theory

description: Validation of the Bipolar Disorder Etiology Scale based on Psychological Behaviorism Theory and Factors Related to the Onset of Bipolar Disorder
DOI: 10.6084/m9.figshare.1255029
title: Altered promoter nucleosome positioning is an early event in gene silencing

description: Gene silencing in cancer frequently involves hypermethylation and dense nucleosome occupancy across promoter regions. How a promoter transitions to this silent state is unclear. Using colorectal adenomas, we investigated nucleosome positioning, DNA methylation, and gene expression in the early stages of gene silencing. Genome-wide gene expression correlated with highly positioned nucleosomes upstream and downstream of a nucleosome-depleted transcription start site (TSS). Hypermethylated promoters displayed increased nucleosome occupancy, specifically at the TSS. We investigated 2 genes, <i>CDH1</i> and <i>CDKN2B</i>, which were silenced in adenomas but lacked promoter hypermethylation. Instead, silencing correlated with loss of nucleosomes from the -2 position upstream of the TSS relative to normal mucosa. In contrast, permanent <i>CDH1</i> silencing in carcinoma cells was characterized by promoter hypermethylation and dense nucleosome occupancy. Our findings suggest that silenced genes transition through an intermediary stage involving altered promoter nucleosome positioning, before permanent silencing by hypermethylation and dense nucleosome occupancy.
DOI: 10.6084/m9.figshare.1255030
title: Using RNA sequencing for identifying gene imprinting and random monoallelic expression in human placenta

description: Given the possible critical importance of placental gene imprinting and random monoallelic expression on fetal and infant health, most of those genes must be identified, in order to understand the risks that the baby might meet during pregnancy and after birth. Therefore, the aim of the current study was to introduce a workflow and tools for analyzing imprinted and random monoallelic gene expression in human placenta, by applying whole-transcriptome (WT) RNA sequencing of placental tissue and genotyping of coding DNA variants in family trios. Ten family trios, each with a healthy spontaneous single-term pregnancy, were recruited. Total RNA was extracted for WT analysis, providing the full sequence information for the placental transcriptome. Parental and child blood DNA genotypes were analyzed by exome SNP genotyping microarrays, mapping the inheritance and estimating the abundance of parental expressed alleles. Imprinted genes showed consistent expression from either parental allele, as demonstrated by the SNP content of sequenced transcripts, while monoallelically expressed genes had random activity of parental alleles. We revealed 4 novel possible imprinted genes (<i>LGALS8</i>, <i>LGALS14</i>, <i>PAPPA2</i> and <i>SPTLC3</i>) and confirmed the imprinting of 4 genes (<i>AIM1</i>, <i>PEG10</i>, <i>RHOBTB3</i> and <i>ZFAT-AS1</i>) in human placenta. The major finding was the identification of 4 genes (<i>ABP1</i>, <i>BCLAF1</i>, <i>IFI30</i> and <i>ZFAT</i>) with random allelic bias, expressing one of the parental alleles preferentially. The main functions of the imprinted and monoallelically expressed genes included: i) mediating cellular apoptosis and tissue development; ii) regulating inflammation and immune system; iii) facilitating metabolic processes; and iv) regulating cell cycle.
DOI: 10.6084/m9.figshare.1255028
title: Cell line differences in replication timing of human glutamate receptor genes and other large genes associated with neural disease

description: There is considerable current interest in the function of epigenetic mechanisms in neuroplasticity with regard to learning and memory formation and to a range of neural diseases. Previously, we described replication timing on human chromosome 21q in the THP-1 human cell line (2n = 46, XY) and showed that several genes associated with neural diseases, such as the neuronal glutamate receptor subunit GluR-5 (<i>GRIK1</i>) and amyloid precursor protein (<i>APP</i>), were located in regions where replication timing transitioned from early to late S phase. Here, we compared replication timing of all known human glutamate receptor genes (26 genes in total) and <i>APP</i> in 6 different human cell lines including human neuron-related cell lines. Replication timings were obtained by integrating our previously reported data with new data generated here and information from the online database ReplicationDomain. We found that many of the glutamate receptor genes were clearly located in replication timing transition zones in neural precursor cells, but this relationship was less clear in embryonic stem cells before neural differentiation; in the latter, the genes were often located in later replication timing zones that displayed DNA hypermethylation. Analysis of selected large glutamate receptor genes (&gt;200 kb), and of <i>APP</i>, showed that their precise replication timing patterns differed among the cell lines. We propose that the transition zones of DNA replication timing are altered by epigenetic mechanisms, and that these changes may affect the neuroplasticity that is important to memory and learning, and may also have a role in the development of neural diseases.
DOI: 10.6084/m9.figshare.1255042.v3
title: Supplement figures for the motivational IAT otivational IAT

description: Supplement material for: Kraus, A. A. & Scholderer, J. (conditional accepted). Indirect measurement of motivation: Developing and testing a motivational Recoding-Free Implicit Association Test (m-IAT-RF).
DOI: 10.6084/m9.figshare.1255029.v1
title: Altered promoter nucleosome positioning is an early event in gene silencing

description: Gene silencing in cancer frequently involves hypermethylation and dense nucleosome occupancy across promoter regions. How a promoter transitions to this silent state is unclear. Using colorectal adenomas, we investigated nucleosome positioning, DNA methylation, and gene expression in the early stages of gene silencing. Genome-wide gene expression correlated with highly positioned nucleosomes upstream and downstream of a nucleosome-depleted transcription start site (TSS). Hypermethylated promoters displayed increased nucleosome occupancy, specifically at the TSS. We investigated 2 genes, <i>CDH1</i> and <i>CDKN2B</i>, which were silenced in adenomas but lacked promoter hypermethylation. Instead, silencing correlated with loss of nucleosomes from the -2 position upstream of the TSS relative to normal mucosa. In contrast, permanent <i>CDH1</i> silencing in carcinoma cells was characterized by promoter hypermethylation and dense nucleosome occupancy. Our findings suggest that silenced genes transition through an intermediary stage involving altered promoter nucleosome positioning, before permanent silencing by hypermethylation and dense nucleosome occupancy.
DOI: 10.6084/m9.figshare.1255042.v4
title: Supplement figures for D-scores of motivational IATs and validation criteria

description: Supplement material for: Kraus, A. A. & Scholderer, J. (conditional accepted). Indirect measurement of motivation: Developing and testing a motivational Recoding-Free Implicit Association Test (m-IAT-RF).
DOI: 10.6084/m9.figshare.1255029.v3
title: Altered promoter nucleosome positioning is an early event in gene silencing

description: Gene silencing in cancer frequently involves hypermethylation and dense nucleosome occupancy across promoter regions. How a promoter transitions to this silent state is unclear. Using colorectal adenomas, we investigated nucleosome positioning, DNA methylation, and gene expression in the early stages of gene silencing. Genome-wide gene expression correlated with highly positioned nucleosomes upstream and downstream of a nucleosome-depleted transcription start site (TSS). Hypermethylated promoters displayed increased nucleosome occupancy, specifically at the TSS. We investigated 2 genes, <i>CDH1</i> and <i>CDKN2B</i>, which were silenced in adenomas but lacked promoter hypermethylation. Instead, silencing correlated with loss of nucleosomes from the -2 position upstream of the TSS relative to normal mucosa. In contrast, permanent <i>CDH1</i> silencing in carcinoma cells was characterized by promoter hypermethylation and dense nucleosome occupancy. Our findings suggest that silenced genes transition through an intermediary stage involving altered promoter nucleosome positioning, before permanent silencing by hypermethylation and dense nucleosome occupancy.
DOI: 10.6084/m9.figshare.1255030.v1
title: Using RNA sequencing for identifying gene imprinting and random monoallelic expression in human placenta

description: Given the possible critical importance of placental gene imprinting and random monoallelic expression on fetal and infant health, most of those genes must be identified, in order to understand the risks that the baby might meet during pregnancy and after birth. Therefore, the aim of the current study was to introduce a workflow and tools for analyzing imprinted and random monoallelic gene expression in human placenta, by applying whole-transcriptome (WT) RNA sequencing of placental tissue and genotyping of coding DNA variants in family trios. Ten family trios, each with a healthy spontaneous single-term pregnancy, were recruited. Total RNA was extracted for WT analysis, providing the full sequence information for the placental transcriptome. Parental and child blood DNA genotypes were analyzed by exome SNP genotyping microarrays, mapping the inheritance and estimating the abundance of parental expressed alleles. Imprinted genes showed consistent expression from either parental allele, as demonstrated by the SNP content of sequenced transcripts, while monoallelically expressed genes had random activity of parental alleles. We revealed 4 novel possible imprinted genes (<i>LGALS8</i>, <i>LGALS14</i>, <i>PAPPA2</i> and <i>SPTLC3</i>) and confirmed the imprinting of 4 genes (<i>AIM1</i>, <i>PEG10</i>, <i>RHOBTB3</i> and <i>ZFAT-AS1</i>) in human placenta. The major finding was the identification of 4 genes (<i>ABP1</i>, <i>BCLAF1</i>, <i>IFI30</i> and <i>ZFAT</i>) with random allelic bias, expressing one of the parental alleles preferentially. The main functions of the imprinted and monoallelically expressed genes included: i) mediating cellular apoptosis and tissue development; ii) regulating inflammation and immune system; iii) facilitating metabolic processes; and iv) regulating cell cycle.
DOI: 10.6084/m9.figshare.1255028.v1
title: Cell line differences in replication timing of human glutamate receptor genes and other large genes associated with neural disease

description: There is considerable current interest in the function of epigenetic mechanisms in neuroplasticity with regard to learning and memory formation and to a range of neural diseases. Previously, we described replication timing on human chromosome 21q in the THP-1 human cell line (2n = 46, XY) and showed that several genes associated with neural diseases, such as the neuronal glutamate receptor subunit GluR-5 (<i>GRIK1</i>) and amyloid precursor protein (<i>APP</i>), were located in regions where replication timing transitioned from early to late S phase. Here, we compared replication timing of all known human glutamate receptor genes (26 genes in total) and <i>APP</i> in 6 different human cell lines including human neuron-related cell lines. Replication timings were obtained by integrating our previously reported data with new data generated here and information from the online database ReplicationDomain. We found that many of the glutamate receptor genes were clearly located in replication timing transition zones in neural precursor cells, but this relationship was less clear in embryonic stem cells before neural differentiation; in the latter, the genes were often located in later replication timing zones that displayed DNA hypermethylation. Analysis of selected large glutamate receptor genes (&gt;200 kb), and of <i>APP</i>, showed that their precise replication timing patterns differed among the cell lines. We propose that the transition zones of DNA replication timing are altered by epigenetic mechanisms, and that these changes may affect the neuroplasticity that is important to memory and learning, and may also have a role in the development of neural diseases.
DOI: 10.6084/m9.figshare.1255029.v2
title: Altered promoter nucleosome positioning is an early event in gene silencing

description: Gene silencing in cancer frequently involves hypermethylation and dense nucleosome occupancy across promoter regions. How a promoter transitions to this silent state is unclear. Using colorectal adenomas, we investigated nucleosome positioning, DNA methylation, and gene expression in the early stages of gene silencing. Genome-wide gene expression correlated with highly positioned nucleosomes upstream and downstream of a nucleosome-depleted transcription start site (TSS). Hypermethylated promoters displayed increased nucleosome occupancy, specifically at the TSS. We investigated 2 genes, <i>CDH1</i> and <i>CDKN2B</i>, which were silenced in adenomas but lacked promoter hypermethylation. Instead, silencing correlated with loss of nucleosomes from the -2 position upstream of the TSS relative to normal mucosa. In contrast, permanent <i>CDH1</i> silencing in carcinoma cells was characterized by promoter hypermethylation and dense nucleosome occupancy. Our findings suggest that silenced genes transition through an intermediary stage involving altered promoter nucleosome positioning, before permanent silencing by hypermethylation and dense nucleosome occupancy.
DOI: 10.6084/m9.figshare.1255042.v6
title: Three supplement figures illustrating D-scores of motivational IATs and validation criteria within two studies

description: Supplement material for: Kraus, A. A. & Scholderer, J. (conditional accepted). Indirect measurement of motivation: Developing and testing a motivational Recoding-Free Implicit Association Test (m-IAT-RF).
DOI: 10.6084/m9.figshare.1255028.v3
title: Cell line differences in replication timing of human glutamate receptor genes and other large genes associated with neural disease

description: There is considerable current interest in the function of epigenetic mechanisms in neuroplasticity with regard to learning and memory formation and to a range of neural diseases. Previously, we described replication timing on human chromosome 21q in the THP-1 human cell line (2n = 46, XY) and showed that several genes associated with neural diseases, such as the neuronal glutamate receptor subunit GluR-5 (<i>GRIK1</i>) and amyloid precursor protein (<i>APP</i>), were located in regions where replication timing transitioned from early to late S phase. Here, we compared replication timing of all known human glutamate receptor genes (26 genes in total) and <i>APP</i> in 6 different human cell lines including human neuron-related cell lines. Replication timings were obtained by integrating our previously reported data with new data generated here and information from the online database ReplicationDomain. We found that many of the glutamate receptor genes were clearly located in replication timing transition zones in neural precursor cells, but this relationship was less clear in embryonic stem cells before neural differentiation; in the latter, the genes were often located in later replication timing zones that displayed DNA hypermethylation. Analysis of selected large glutamate receptor genes (&gt;200 kb), and of <i>APP</i>, showed that their precise replication timing patterns differed among the cell lines. We propose that the transition zones of DNA replication timing are altered by epigenetic mechanisms, and that these changes may affect the neuroplasticity that is important to memory and learning, and may also have a role in the development of neural diseases.
DOI: 10.6084/m9.figshare.1255042.v5
title: Three supplement figures illustrating D-scores of motivational IATs wi validation criteria

description: Supplement material for: Kraus, A. A. & Scholderer, J. (conditional accepted). Indirect measurement of motivation: Developing and testing a motivational Recoding-Free Implicit Association Test (m-IAT-RF).
DOI: 10.6084/m9.figshare.1255030.v2
title: Using RNA sequencing for identifying gene imprinting and random monoallelic expression in human placenta

description: Given the possible critical importance of placental gene imprinting and random monoallelic expression on fetal and infant health, most of those genes must be identified, in order to understand the risks that the baby might meet during pregnancy and after birth. Therefore, the aim of the current study was to introduce a workflow and tools for analyzing imprinted and random monoallelic gene expression in human placenta, by applying whole-transcriptome (WT) RNA sequencing of placental tissue and genotyping of coding DNA variants in family trios. Ten family trios, each with a healthy spontaneous single-term pregnancy, were recruited. Total RNA was extracted for WT analysis, providing the full sequence information for the placental transcriptome. Parental and child blood DNA genotypes were analyzed by exome SNP genotyping microarrays, mapping the inheritance and estimating the abundance of parental expressed alleles. Imprinted genes showed consistent expression from either parental allele, as demonstrated by the SNP content of sequenced transcripts, while monoallelically expressed genes had random activity of parental alleles. We revealed 4 novel possible imprinted genes (<i>LGALS8</i>, <i>LGALS14</i>, <i>PAPPA2</i> and <i>SPTLC3</i>) and confirmed the imprinting of 4 genes (<i>AIM1</i>, <i>PEG10</i>, <i>RHOBTB3</i> and <i>ZFAT-AS1</i>) in human placenta. The major finding was the identification of 4 genes (<i>ABP1</i>, <i>BCLAF1</i>, <i>IFI30</i> and <i>ZFAT</i>) with random allelic bias, expressing one of the parental alleles preferentially. The main functions of the imprinted and monoallelically expressed genes included: i) mediating cellular apoptosis and tissue development; ii) regulating inflammation and immune system; iii) facilitating metabolic processes; and iv) regulating cell cycle.
DOI: 10.6084/m9.figshare.1255024
title: Cigarette smoking reduces DNA methylation levels at multiple genomic loci but the effect is partially reversible upon cessation

description: Smoking is a major risk factor in many diseases. Genome wide association studies have linked genes for nicotine dependence and smoking behavior to increased risk of cardiovascular, pulmonary, and malignant diseases. We conducted an epigenome wide association study in peripheral-blood DNA in 464 individuals (22 current smokers and 263 ex-smokers), using the Human Methylation 450 K array. Upon replication in an independent sample of 356 twins (41 current and 104 ex-smokers), we identified 30 probes in 15 distinct loci, all of which reached genome-wide significance in the combined analysis <i>P</i> &lt; 5 × 10<sup>−8</sup>. All but one probe (cg17024919) remained significant after adjusting for blood cell counts. We replicated all 9 known loci and found an independent signal at <i>CPOX</i> near <i>GPR15.</i> In addition, we found 6 new loci at <i>PRSS23</i>, <i>AVPR1B</i>, <i>PSEN2</i>, <i>LINC00299</i>, <i>RPS6KA2,</i> and <i>KIAA0087.</i> Most of the lead probes (13 out of 15) associated with cigarette smoking, overlapped regions of open chromatin (FAIRE and DNaseI hypersensitive sites) or / and H3K27Ac peaks (ENCODE data set), which mark regulatory elements. The effect of smoking on DNA methylation was partially reversible upon smoking cessation for longer than 3 months. We report the first statistically significant interaction between a SNP (rs2697768) and cigarette smoking on DNA methylation (cg03329539). We provide evidence that the metSNP for cg03329539 regulates expression of the <i>CHRND</i> gene located circa 95 Kb downstream of the methylation site. Our findings suggest the existence of dynamic, reversible site-specific methylation changes in response to cigarette smoking , which may contribute to the extended health risks associated with cigarette smoking.