cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1409398.v244
title: ABO phenotype protected reproduction as it is based on fucosylations.

description: The molecular biological relationship between human fertility and ABO(H) blood group phenotype formation becomes evident with the rare (Oh) or <i>Bombay</i> blood type, which, based on the history of his own family, Charles Darwin would have interpreted as resulting from reduced fertility in consanguinities. In its native form, the <i>Bombay</i> type occurs in individuals with an extremely rare genotype (h/h;se/se), by which the fucosyltransferases FUT1 and FUT2 are not produced due to point mutations. These enzymes, encoded on chromosome 19, are epistatically connected with the A and B allelic glycotransferase functions encoded on chromosome 9, while the fucosyl residues provide the functional-structural basis for the formation of any ABO(H) phenotype on the cell surface or in secretions and plasma proteins. Immunoglobulins are also heavily fucosylated, and via developmental variation in the positions between the cell surfaces and the heavy chains of immunoglobulins, fucosyl residues appear to augment or reduce antibody-mediated cellular cytotoxicity involving physiological anti-self-reactivity; moreover, by regulating the assembly and intracellular signaling of precursor B cell receptors, the core fucosylation of immunoglobulin heavy chains represents a key mechanism in clonal selection. In fact, the seminal plasma of leukospermic infertile men has been reported to exert high levels of poorly core-fucosylated IgG. Consequently, in <i>Bombay </i>type individuals, non-somatic glycosylation processes of embryogenic stem cell-to-germ cell transformation, which involve the modification and <i>O</i>-fucosylation of epidermal growth factor (EGF), are most likely exposed to metabolic competition with multiple glycosidic sites of poorly fucosylated, glycan-depleted immunoglobulins promoting anti-self-reactive cellular cytotoxicity in male gamete performance.
DOI: 10.6084/m9.figshare.1397535.v1
title: Biochemical fractionation of soil organic matter after incorporation of organic residues

description: Description will come when the associated paper will be published.
DOI: 10.6084/m9.figshare.1397533
title: Wikipedia Content Volatility

description: Paper Abstract: Wikipedia has quickly become one of the most frequently accessed encyclopedic references, despite the ease with which content can be changed and the potential for ‘edit wars’ surrounding controversial topics. Little is known about how this potential for controversy affects the accuracy and stability of information on scientific topics, especially those with associated political controversy. Here we present an analysis of the Wikipedia edit histories for seven scientific articles and show that topics we consider politically but not scientifically “controversial” (such as evolution and global warming) experience more frequent edits with more words changed per day than pages we consider “noncontroversial” (such as the standard model in physics or heliocentrism). For example, over the period we analyzed, the global warming page was edited on average (geometric mean ±SD) 1.9±2.7 times resulting in 110.9±10.3 words changed per day, while the standard model in physics was only edited 0.2±1.4 times resulting in 9.4±5.0 words changed per day. The high rate of change observed in these pages makes it difficult for experts to monitor accuracy and contribute time-consuming corrections, to the possible detriment of scientific accuracy. As our society turns to Wikipedia as a primary source of scientific information, it is vital we read it critically and with the understanding that the content is dynamic and vulnerable to vandalism and other shenanigans. Notes: For full explanation of data contained in files refer to the Wikireview_DataCollect.R file which was used to assemble the data. For the wordschanged.csv file, refer to the output of the wdiff function (http://www.gnu.org/software/wdiff/) for more details.
DOI: 10.6084/m9.figshare.1397543.v2
title: An aromatic cage is required but not sufficient for binding of Tudor domains of the Polycomblike protein family to H3K36me3

description: Polycomblike (Pcl) proteins are important transcriptional regulators and components of the Polycomb Repressive Complex 2 (PRC2). The Tudor domains of human homologs PHF1 and PHF19 have been found to recognize trimethylated lysine 36 of histone H3 (H3K36me3); however, the biological role of Tudor domains of other Pcl proteins remains poorly understood. Here, we characterize the molecular basis underlying histone binding activities of the Tudor domains of the Pcl family. In contrast to a predominant view, we found that the methyl lysine-binding aromatic cage is necessary but not sufficient for recognition of H3K36me3 by these Tudor domains and that a hydrophobic patch, adjacent to the aromatic cage, is also required.
DOI: 10.6084/m9.figshare.1397544.v4
title: VRK1 chromatin kinase phosphorylates H2AX and is required for foci formation induced by DNA damage

description: All types of DNA damage cause a local alteration and relaxation of chromatin structure. Sensing and reacting to this initial chromatin alteration is a necessary trigger for any type of DNA damage response (DDR). In this context, chromatin kinases are likely candidates to participate in detection and reaction to a locally altered chromatin as a consequence of DNA damage and, thus, initiate the appropriate cellular response. In this work, we demonstrate that VRK1 is a nucleosomal chromatin kinase and that its depletion causes loss of histones H3 and H4 acetylation, which are required for chromatin relaxation, both in basal conditions and after DNA damage, independently of ATM. Moreover, VRK1 directly and stably interacts with histones H2AX and H3 in basal conditions. In response to DNA damage induced by ionizing radiation, histone H2AX is phosphorylated in Ser139 by VRK1. The phosphorylation of H2AX and the formation of γH2AX foci induced by ionizing radiation (IR), are prevented by VRK1 depletion and are rescued by kinase-active, but not kinase-dead, VRK1. In conclusion, we found that VRK1 is a novel chromatin component that reacts to its alterations and participates very early in DDR, functioning by itself or in cooperation with ATM.
DOI: 10.6084/m9.figshare.1397533.v1
title: Wikipedia Content Volatility

description: Paper Abstract: Wikipedia has quickly become one of the most frequently accessed encyclopedic references, despite the ease with which content can be changed and the potential for ‘edit wars’ surrounding controversial topics. Little is known about how this potential for controversy affects the accuracy and stability of information on scientific topics, especially those with associated political controversy. Here we present an analysis of the Wikipedia edit histories for seven scientific articles and show that topics we consider politically but not scientifically “controversial” (such as evolution and global warming) experience more frequent edits with more words changed per day than pages we consider “noncontroversial” (such as the standard model in physics or heliocentrism). For example, over the period we analyzed, the global warming page was edited on average (geometric mean ±SD) 1.9±2.7 times resulting in 110.9±10.3 words changed per day, while the standard model in physics was only edited 0.2±1.4 times resulting in 9.4±5.0 words changed per day. The high rate of change observed in these pages makes it difficult for experts to monitor accuracy and contribute time-consuming corrections, to the possible detriment of scientific accuracy. As our society turns to Wikipedia as a primary source of scientific information, it is vital we read it critically and with the understanding that the content is dynamic and vulnerable to vandalism and other shenanigans. Notes: For full explanation of data contained in files refer to the Wikireview_DataCollect.R file which was used to assemble the data. For the wordschanged.csv file, refer to the output of the wdiff function (http://www.gnu.org/software/wdiff/) for more details.
DOI: 10.6084/m9.figshare.1397542.v2
title: Differential DNA methylation in umbilical cord blood of infants exposed to mercury and arsenic <i>in utero</i>

description: Mercury and arsenic are known developmental toxicants. Prenatal exposures are associated with adverse childhood health outcomes that could be in part mediated by epigenetic alterations that may also contribute to altered immune profiles. In this study, we examined the association between prenatal mercury exposure on both DNA methylation and white blood cell composition of cord blood, and evaluated the interaction with prenatal arsenic exposure. A total of 138 mother-infant pairs with postpartum maternal toenail mercury, prenatal urinary arsenic concentrations, and newborn cord blood were assessed using the Illumina Infinium Methylation450 array. White blood cell composition was inferred from DNA methylation measurements. A doubling in toenail mercury concentration was associated with a 2.5% decrease (95% CI: 5.0%, 1.0%) in the estimated monocyte proportion. An increase of 3.5% (95% CI: 1.0, 7.0) in B-cell proportion was observed for females only. Among the top 100 CpGs associated with toenail mercury levels (ranked on <i>P-value</i>), there was a significant enrichment of loci located in North shore regions of CpG islands (<i>P</i> = 0.049), and the majority of these loci were hypermethylated (85%). Among the top 100 CpGs for the interaction between arsenic and mercury, there was a greater than expected proportion of loci located in CpG islands (<i>P</i> = 0.045) and in South shore regions (<i>P</i> = 0.009) and all of these loci were hypermethylated. This work supports the hypothesis that mercury may be contributing to epigenetic variability and immune cell proportion changes, and suggests that <i>in utero</i> exposure to mercury and arsenic, even at low levels, may interact to impact the epigenome.
DOI: 10.6084/m9.figshare.1409398.v245
title: ABO phenotype protected reproduction as it is based on fucosylations.

description: The molecular biological relationship between human fertility and ABO(H) blood group phenotype formation becomes evident with the rare (Oh) or <i>Bombay</i> blood type, which, based on the history of his own family, Charles Darwin would have interpreted as resulting from reduced fertility in consanguinities. In its native form, the <i>Bombay</i> type occurs in individuals with an extremely rare genotype (h/h;se/se), by which the fucosyltransferases FUT1 and FUT2 are not produced due to point mutations. These enzymes, encoded on chromosome 19, are epistatically connected with the A and B allelic glycotransferase functions encoded on chromosome 9, while the fucosyl residues provide the functional-structural basis for the formation of any ABO(H) phenotype on the cell surface or in secretions and plasma proteins. Immunoglobulins are also heavily fucosylated, and via developmental variation in the positions between the cell surfaces and the heavy chains of immunoglobulins, fucosyl residues appear to augment or reduce antibody-mediated cellular cytotoxicity involving physiological anti-self-reactivity; moreover, by regulating the assembly and intracellular signaling of precursor B cell receptors, the core fucosylation of immunoglobulin heavy chains represents a key mechanism in clonal selection. In fact, the seminal plasma of leukospermic infertile men has been reported to exert high levels of poorly core-fucosylated IgG. Consequently, in <i>Bombay </i>type individuals, non-somatic glycosylation processes of embryogenic stem cell-to-germ cell transformation, which involve the modification and <i>O</i>-fucosylation of epidermal growth factor (EGF), are most likely exposed to metabolic competition with multiple glycosidic sites of poorly fucosylated, glycan-depleted immunoglobulins promoting anti-self-reactive cellular cytotoxicity in male gamete performance.
DOI: 10.6084/m9.figshare.1397544.v3
title: VRK1 chromatin kinase phosphorylates H2AX and is required for foci formation induced by DNA damage

description: All types of DNA damage cause a local alteration and relaxation of chromatin structure. Sensing and reacting to this initial chromatin alteration is a necessary trigger for any type of DNA damage response (DDR). In this context, chromatin kinases are likely candidates to participate in detection and reaction to a locally altered chromatin as a consequence of DNA damage and, thus, initiate the appropriate cellular response. In this work, we demonstrate that VRK1 is a nucleosomal chromatin kinase and that its depletion causes loss of histones H3 and H4 acetylation, which are required for chromatin relaxation, both in basal conditions and after DNA damage, independently of ATM. Moreover, VRK1 directly and stably interacts with histones H2AX and H3 in basal conditions. In response to DNA damage induced by ionizing radiation, histone H2AX is phosphorylated in Ser139 by VRK1. The phosphorylation of H2AX and the formation of γH2AX foci induced by ionizing radiation (IR), are prevented by VRK1 depletion and are rescued by kinase-active, but not kinase-dead, VRK1. In conclusion, we found that VRK1 is a novel chromatin component that reacts to its alterations and participates very early in DDR, functioning by itself or in cooperation with ATM.
DOI: 10.6084/m9.figshare.1397542.v3
title: Differential DNA methylation in umbilical cord blood of infants exposed to mercury and arsenic <i>in utero</i>

description: Mercury and arsenic are known developmental toxicants. Prenatal exposures are associated with adverse childhood health outcomes that could be in part mediated by epigenetic alterations that may also contribute to altered immune profiles. In this study, we examined the association between prenatal mercury exposure on both DNA methylation and white blood cell composition of cord blood, and evaluated the interaction with prenatal arsenic exposure. A total of 138 mother-infant pairs with postpartum maternal toenail mercury, prenatal urinary arsenic concentrations, and newborn cord blood were assessed using the Illumina Infinium Methylation450 array. White blood cell composition was inferred from DNA methylation measurements. A doubling in toenail mercury concentration was associated with a 2.5% decrease (95% CI: 5.0%, 1.0%) in the estimated monocyte proportion. An increase of 3.5% (95% CI: 1.0, 7.0) in B-cell proportion was observed for females only. Among the top 100 CpGs associated with toenail mercury levels (ranked on <i>P-value</i>), there was a significant enrichment of loci located in North shore regions of CpG islands (<i>P</i> = 0.049), and the majority of these loci were hypermethylated (85%). Among the top 100 CpGs for the interaction between arsenic and mercury, there was a greater than expected proportion of loci located in CpG islands (<i>P</i> = 0.045) and in South shore regions (<i>P</i> = 0.009) and all of these loci were hypermethylated. This work supports the hypothesis that mercury may be contributing to epigenetic variability and immune cell proportion changes, and suggests that <i>in utero</i> exposure to mercury and arsenic, even at low levels, may interact to impact the epigenome.
DOI: 10.6084/m9.figshare.1397543.v3
title: An aromatic cage is required but not sufficient for binding of Tudor domains of the Polycomblike protein family to H3K36me3

description: Polycomblike (Pcl) proteins are important transcriptional regulators and components of the Polycomb Repressive Complex 2 (PRC2). The Tudor domains of human homologs PHF1 and PHF19 have been found to recognize trimethylated lysine 36 of histone H3 (H3K36me3); however, the biological role of Tudor domains of other Pcl proteins remains poorly understood. Here, we characterize the molecular basis underlying histone binding activities of the Tudor domains of the Pcl family. In contrast to a predominant view, we found that the methyl lysine-binding aromatic cage is necessary but not sufficient for recognition of H3K36me3 by these Tudor domains and that a hydrophobic patch, adjacent to the aromatic cage, is also required.
DOI: 10.6084/m9.figshare.1409398.v246
title: ABO phenotype protected reproduction as it is based on fucosylations.

description: The molecular biological relationship between human fertility and ABO(H) blood group phenotype formation becomes evident with the rare (Oh) or <i>Bombay</i> blood type, which, based on the history of his own family, Charles Darwin would have interpreted as resulting from reduced fertility in consanguinities. In its native form, the <i>Bombay</i> type occurs in individuals with an extremely rare genotype (h/h;se/se), by which the fucosyltransferases FUT1 and FUT2 are not produced due to point mutations. These enzymes, encoded on chromosome 19, are epistatically connected with the A and B allelic glycotransferase functions encoded on chromosome 9, while the fucosyl residues provide the functional-structural basis for the formation of any ABO(H) phenotype on the cell surface or in secretions and plasma proteins. Immunoglobulins are also heavily fucosylated, and via developmental variation in the positions between the cell surfaces and the heavy chains of immunoglobulins, fucosyl residues appear to augment or reduce antibody-mediated cellular cytotoxicity involving physiological anti-self-reactivity; moreover, by regulating the assembly and intracellular signaling of precursor B cell receptors, the core fucosylation of immunoglobulin heavy chains represents a key mechanism in clonal selection. In fact, the seminal plasma of leukospermic infertile men has been reported to exert high levels of poorly core-fucosylated IgG. Consequently, in <i>Bombay </i>type individuals, non-somatic glycosylation processes of embryogenic stem cell-to-germ cell transformation, which involve the modification and <i>O</i>-fucosylation of epidermal growth factor (EGF), are most likely exposed to metabolic competition with multiple glycosidic sites of poorly fucosylated, glycan-depleted immunoglobulins promoting anti-self-reactive cellular cytotoxicity in male gamete performance.
DOI: 10.6084/m9.figshare.1397542.v5
title: Differential DNA methylation in umbilical cord blood of infants exposed to mercury and arsenic <i>in utero</i>

description: Mercury and arsenic are known developmental toxicants. Prenatal exposures are associated with adverse childhood health outcomes that could be in part mediated by epigenetic alterations that may also contribute to altered immune profiles. In this study, we examined the association between prenatal mercury exposure on both DNA methylation and white blood cell composition of cord blood, and evaluated the interaction with prenatal arsenic exposure. A total of 138 mother-infant pairs with postpartum maternal toenail mercury, prenatal urinary arsenic concentrations, and newborn cord blood were assessed using the Illumina Infinium Methylation450 array. White blood cell composition was inferred from DNA methylation measurements. A doubling in toenail mercury concentration was associated with a 2.5% decrease (95% CI: 5.0%, 1.0%) in the estimated monocyte proportion. An increase of 3.5% (95% CI: 1.0, 7.0) in B-cell proportion was observed for females only. Among the top 100 CpGs associated with toenail mercury levels (ranked on <i>P-value</i>), there was a significant enrichment of loci located in North shore regions of CpG islands (<i>P</i> = 0.049), and the majority of these loci were hypermethylated (85%). Among the top 100 CpGs for the interaction between arsenic and mercury, there was a greater than expected proportion of loci located in CpG islands (<i>P</i> = 0.045) and in South shore regions (<i>P</i> = 0.009) and all of these loci were hypermethylated. This work supports the hypothesis that mercury may be contributing to epigenetic variability and immune cell proportion changes, and suggests that <i>in utero</i> exposure to mercury and arsenic, even at low levels, may interact to impact the epigenome.
DOI: 10.6084/m9.figshare.1397502
title: Supplemental Materials to submitted paper

description: This file contains the supplemental materials to the paper: <em>Esteban O. et al., Surface-driven registration method for the structure-informed segmentation of diffusion MR images. NeuroImage (accepted), 2016. </em><em>doi: http://dx.doi.org/10.1016/j.neuroimage.2016.05.011</em><em><br></em> <strong>Abstract:</strong> Current methods for processing diffusion MRI (dMRI) to map the connectivity of the human brain require precise delineations of anatomical structures. This requirement has been approached either segmenting the data in native dMRI space or mapping the structural information from T1-weighted (T1w) images. The characteristic features of diffusion data in terms of signal-to-noise ratio, resolution, as well as the geometrical distortions caused by the inhomogeneity of magnetic susceptibility across tissues hinder both solutions. Unifying the two approaches, we propose regseg, a surface-to-volume nonlinear registration method that segments homogeneous regions within multivariate images by mapping a set of nested reference-surfaces. Accurate surfaces are extracted from a T1w image of the subject, using as target image the bivariate volume comprehending the fractional anisotropy (FA) and the apparent diffusion coefficient (ADC) maps derived from the dMRI dataset. We first verify the accuracy of regseg on a general context using digital phantoms. Then we establish an evaluation framework using undistorted dMRI data from the Human Connectome Project (HCP) and known deformations derived from real inhomogeneity fieldmaps. We analyze the performance of regseg computing the misregistration error of the surfaces estimated after being mapped with regseg onto 16 datasets from the HCP. The distribution of errors shows a 95% CI of 0.56–0.66 mm, that is below the dMRI resolution (1.25 mm, isotropic). Finally, we cross-compare the proposed tool against a nonlinear b0-to-T2w registration method, thereby obtaining a significantly lower misregistration error with<br>regseg. Therefore, we demonstrate that regseg allows the accurate mapping of structural information in dMRI space, enabling the application of new structure-informed techniques in the connectome extraction.
DOI: 10.6084/m9.figshare.1397543.v5
title: An aromatic cage is required but not sufficient for binding of Tudor domains of the Polycomblike protein family to H3K36me3

description: Polycomblike (Pcl) proteins are important transcriptional regulators and components of the Polycomb Repressive Complex 2 (PRC2). The Tudor domains of human homologs PHF1 and PHF19 have been found to recognize trimethylated lysine 36 of histone H3 (H3K36me3); however, the biological role of Tudor domains of other Pcl proteins remains poorly understood. Here, we characterize the molecular basis underlying histone binding activities of the Tudor domains of the Pcl family. In contrast to a predominant view, we found that the methyl lysine-binding aromatic cage is necessary but not sufficient for recognition of H3K36me3 by these Tudor domains and that a hydrophobic patch, adjacent to the aromatic cage, is also required.
DOI: 10.6084/m9.figshare.1397543.v4
title: An aromatic cage is required but not sufficient for binding of Tudor domains of the Polycomblike protein family to H3K36me3

description: Polycomblike (Pcl) proteins are important transcriptional regulators and components of the Polycomb Repressive Complex 2 (PRC2). The Tudor domains of human homologs PHF1 and PHF19 have been found to recognize trimethylated lysine 36 of histone H3 (H3K36me3); however, the biological role of Tudor domains of other Pcl proteins remains poorly understood. Here, we characterize the molecular basis underlying histone binding activities of the Tudor domains of the Pcl family. In contrast to a predominant view, we found that the methyl lysine-binding aromatic cage is necessary but not sufficient for recognition of H3K36me3 by these Tudor domains and that a hydrophobic patch, adjacent to the aromatic cage, is also required.