cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.4225/03/56f9e13d29762
title: The Personal Library of Luigi Capuana

description: This dataset consists of a spreadsheet containing details of the personal library of the Sicilian Author Luigi Capuana (1839-1915) as maintained by the Fondo Capuana (Mineo, Sicily). The catalogue gives bibliographic details for the collection; Brian Zuccala and Simon Musgrave have added geodata for the places of publication of the works and some additional information about genre and language. We are using the data for various investigations of the work of Capuana, of which the map stored here is a first example (it shows the places of publication of the items in the library for the European mainland). Added 19/04/2016: A surprising aspect of the data which can be seen in the first map is the amount of material in Capuana's library which was published in Sicily. The second graphic is a network diagram showing the relation between places of publication in Sicily and year of publication. <br>
DOI: 10.6084/m9.figshare.3125773
title: VineShedding_SW Ohio.csv

description: This dataset contains the site location, four letter species code for tree species (first two, genus; second two, species), diameter at breast height, and number of climbing lianas per tree. This work was conducted in the Great Miami River and Little Miami River watersheds of southwestern Ohio, United States.<br><br>Data forms the basis of the manuscript (Northeastern Naturalist): Exfoliating Bark Does Not Protect Platanus occidentalis L. From Root-Climbing Lianas. In press.<br><br>
DOI: 10.6084/m9.figshare.3125773.v1
title: VineShedding_SW Ohio.csv

description: This dataset contains the site location, four letter species code for tree species (first two, genus; second two, species), diameter at breast height, and number of climbing lianas per tree. This work was conducted in the Great Miami River and Little Miami River watersheds of southwestern Ohio, United States.<br><br>Data forms the basis of the manuscript (on bioRxiv): Exfoliating Bark Does Not Protect Platanus occidentalis L. From Root-Climbing Lianas http://dx.doi.org/10.1101/046102 <br><br>
DOI: 10.6084/m9.figshare.3125671
title: <i>Anaplasma phagocytophilum</i> increases the levels of histone modifying enzymes to inhibit cell apoptosis and facilitate pathogen infection in the tick vector <i>Ixodes scapularis</i>

description: Epigenetic mechanisms have not been characterized in ticks despite their importance as vectors of human and animal diseases worldwide. The objective of this study was to characterize the histones and histone modifying enzymes (HMEs) of the tick vector <i>Ixodes scapularis</i> and their role during <i>Anaplasma phagocytophilum</i> infection. We first identified 5 histones and 34 HMEs in <i>I. scapularis</i> in comparison with similar proteins in model organisms. Then, we used transcriptomic and proteomic data to analyze the mRNA and protein levels of <i>I. scapularis</i> histones and HMEs in response to <i>A. phagocytophilum</i> infection of tick tissues and cultured cells. Finally, selected HMEs were functionally characterized by pharmacological studies in cultured tick cells. The results suggest that <i>A. phagocytophilum</i> manipulates tick cell epigenetics to increase <i>I. scapularis</i> p300/CBP, histone deacetylase, and Sirtuin levels, resulting in an inhibition of cell apoptosis that in turn facilitates pathogen infection and multiplication. These results also suggest that a compensatory mechanism might exist by which <i>A. phagocytophilum</i> manipulates tick HMEs to regulate transcription and apoptosis in a tissue-specific manner to facilitate infection, but preserving tick fitness to guarantee survival of both pathogens and ticks. Our study also indicates that the pathogen manipulates arthropod and vertebrate cell epigenetics in similar ways to inhibit the host response to infection. Epigenetic regulation of tick biological processes is an essential element of the infection by <i>A. phagocytophilum</i> and the study of the mechanisms and principal actors involved is likely to provide clues for the development of anti-tick drugs and vaccines.
DOI: 10.6084/m9.figshare.3125671.v1
title: <i>Anaplasma phagocytophilum</i> increases the levels of histone modifying enzymes to inhibit cell apoptosis and facilitate pathogen infection in the tick vector <i>Ixodes scapularis</i>

description: Epigenetic mechanisms have not been characterized in ticks despite their importance as vectors of human and animal diseases worldwide. The objective of this study was to characterize the histones and histone modifying enzymes (HMEs) of the tick vector <i>Ixodes scapularis</i> and their role during <i>Anaplasma phagocytophilum</i> infection. We first identified 5 histones and 34 HMEs in <i>I. scapularis</i> in comparison with similar proteins in model organisms. Then, we used transcriptomic and proteomic data to analyze the mRNA and protein levels of <i>I. scapularis</i> histones and HMEs in response to <i>A. phagocytophilum</i> infection of tick tissues and cultured cells. Finally, selected HMEs were functionally characterized by pharmacological studies in cultured tick cells. The results suggest that <i>A. phagocytophilum</i> manipulates tick cell epigenetics to increase <i>I. scapularis</i> p300/CBP, histone deacetylase, and Sirtuin levels, resulting in an inhibition of cell apoptosis that in turn facilitates pathogen infection and multiplication. These results also suggest that a compensatory mechanism might exist by which <i>A. phagocytophilum</i> manipulates tick HMEs to regulate transcription and apoptosis in a tissue-specific manner to facilitate infection, but preserving tick fitness to guarantee survival of both pathogens and ticks. Our study also indicates that the pathogen manipulates arthropod and vertebrate cell epigenetics in similar ways to inhibit the host response to infection. Epigenetic regulation of tick biological processes is an essential element of the infection by <i>A. phagocytophilum</i> and the study of the mechanisms and principal actors involved is likely to provide clues for the development of anti-tick drugs and vaccines.
DOI: 10.6084/m9.figshare.3125668
title: Maternal genome-wide DNA methylation profiling in gestational diabetes shows distinctive disease-associated changes relative to matched healthy pregnancies

description: Several recent reports have described associations between gestational diabetes (GDM) and changes to the epigenomic landscape where the DNA samples were derived from either cord or placental sources. We employed genome-wide 450K array analysis to determine changes to the epigenome in a unique cohort of maternal blood DNA from 11 pregnant women prior to GDM development relative to matched controls. Hierarchical clustering segregated the samples into 2 distinct clusters comprising GDM and healthy pregnancies. Screening identified 100 CpGs with a mean β-value difference of ≥0.2 between cases and controls. Using stringent criteria, 5 CpGs (within <i>COPS8, PIK3R5, HAAO, CCDC124</i>, and <i>C5orf34</i> genes) demonstrated potentials to be clinical biomarkers as revealed by differential methylation in 8 of 11 women who developed GDM relative to matched controls. We identified, for the first time, maternal methylation changes <i>prior</i> to the onset of GDM that may prove useful as biomarkers for early therapeutic intervention.
DOI: 10.6084/m9.figshare.3125668.v1
title: Maternal genome-wide DNA methylation profiling in gestational diabetes shows distinctive disease-associated changes relative to matched healthy pregnancies

description: Several recent reports have described associations between gestational diabetes (GDM) and changes to the epigenomic landscape where the DNA samples were derived from either cord or placental sources. We employed genome-wide 450K array analysis to determine changes to the epigenome in a unique cohort of maternal blood DNA from 11 pregnant women prior to GDM development relative to matched controls. Hierarchical clustering segregated the samples into 2 distinct clusters comprising GDM and healthy pregnancies. Screening identified 100 CpGs with a mean β-value difference of ≥0.2 between cases and controls. Using stringent criteria, 5 CpGs (within <i>COPS8, PIK3R5, HAAO, CCDC124</i>, and <i>C5orf34</i> genes) demonstrated potentials to be clinical biomarkers as revealed by differential methylation in 8 of 11 women who developed GDM relative to matched controls. We identified, for the first time, maternal methylation changes <i>prior</i> to the onset of GDM that may prove useful as biomarkers for early therapeutic intervention.
DOI: 10.6084/m9.figshare.3125665
title: DNA methylation profiling reveals differences in the 3 human monocyte subsets and identifies uremia to induce DNA methylation changes during differentiation

description: Human monocytes are a heterogeneous cell population consisting of 3 subsets: classical CD14++CD16-, intermediate CD14++CD16+ and nonclassical CD14+CD16++ monocytes. <i>Via</i> poorly characterized mechanisms, intermediate monocyte counts rise in chronic inflammatory diseases, among which chronic kidney disease is of particular epidemiologic importance. DNA methylation is a central epigenetic feature that controls hematopoiesis. By applying next-generation Methyl-Sequencing we now tested how far the 3 monocyte subsets differ in their DNA methylome and whether uremia induces DNA methylation changes in differentiating monocytes. We found that each monocyte subset displays a unique phenotype with regards to DNA methylation. Genes with differentially methylated promoter regions in intermediate monocytes were linked to distinct immunological processes, which is in line with results from recent gene expression analyses. <i>In vitro</i>, uremia induced dysregulation of DNA methylation in differentiating monocytes, which affected several transcription regulators important for monocyte differentiation (e.g., <i>FLT3, HDAC1, MNT</i>) and led to enhanced generation of intermediate monocytes. As potential mediator, the uremic toxin and methylation inhibitor S-adenosylhomocysteine induced shifts in monocyte subsets <i>in vitro</i>, and associated with monocyte subset counts <i>in vivo</i>. Our data support the concept of monocyte trichotomy and the distinct role of intermediate monocytes in human immunity. The shift in monocyte subsets that occurs in chronic kidney disease, a proinflammatory condition of substantial epidemiological impact, may be induced by accumulation of uremic toxins that mediate epigenetic dysregulation.
DOI: 10.6084/m9.figshare.3125623
title: MARITIME LAW: THE ORIGINS AND LEGAL-HISTORICAL EVOLUTION FROM ANTIQUITY TO MORDERN TIME

description: This article aims to make a brief summary of the legal and regulatory developments in maritime law Based on the view that the Law of the Sea , in essence , was forged in customary practices dating back from time immemorial, is studied , the training process right from the usual, as these customs emerged and promoted in aeons to influence the use of modern conceptions and water traffic . It will highlight the eminent influence that the Law of the Sea had for the formation of the present political, economic and legal on a global scale.
DOI: 10.6084/m9.figshare.3125665.v2
title: DNA methylation profiling reveals differences in the 3 human monocyte subsets and identifies uremia to induce DNA methylation changes during differentiation

description: Human monocytes are a heterogeneous cell population consisting of 3 subsets: classical CD14++CD16-, intermediate CD14++CD16+ and nonclassical CD14+CD16++ monocytes. <i>Via</i> poorly characterized mechanisms, intermediate monocyte counts rise in chronic inflammatory diseases, among which chronic kidney disease is of particular epidemiologic importance. DNA methylation is a central epigenetic feature that controls hematopoiesis. By applying next-generation Methyl-Sequencing we now tested how far the 3 monocyte subsets differ in their DNA methylome and whether uremia induces DNA methylation changes in differentiating monocytes. We found that each monocyte subset displays a unique phenotype with regards to DNA methylation. Genes with differentially methylated promoter regions in intermediate monocytes were linked to distinct immunological processes, which is in line with results from recent gene expression analyses. <i>In vitro</i>, uremia induced dysregulation of DNA methylation in differentiating monocytes, which affected several transcription regulators important for monocyte differentiation (e.g., <i>FLT3, HDAC1, MNT</i>) and led to enhanced generation of intermediate monocytes. As potential mediator, the uremic toxin and methylation inhibitor S-adenosylhomocysteine induced shifts in monocyte subsets <i>in vitro</i>, and associated with monocyte subset counts <i>in vivo</i>. Our data support the concept of monocyte trichotomy and the distinct role of intermediate monocytes in human immunity. The shift in monocyte subsets that occurs in chronic kidney disease, a proinflammatory condition of substantial epidemiological impact, may be induced by accumulation of uremic toxins that mediate epigenetic dysregulation.
DOI: 10.6084/m9.figshare.3125665.v1
title: DNA methylation profiling reveals differences in the three human monocyte subsets and identifies uremia to induce DNA methylation changes during differentiation

description: Human monocytes are a heterogeneous cell population consisting of three subsets: classical CD14++CD16-, intermediate CD14++CD16+ and nonclassical CD14+CD16++ monocytes. <i>Via</i> poorly characterized mechanisms, intermediate monocyte counts rise in chronic inflammatory diseases, among which chronic kidney disease is of particular epidemiologic importance. DNA methylation is a central epigenetic feature that controls hematopoiesis. By applying next-generation Methyl-Sequencing we now tested how far the three monocyte subsets differ in their DNA methylome and whether uremia induces DNA methylation changes in differentiating monocytes. We found that each monocyte subset displays a unique phenotype with regards to DNA methylation. Genes with differentially methylated promoter regions in intermediate monocytes were linked to distinct immunological processes, which is in line with results from recent gene expression analyses. <i>In vitro</i>, uremia induced dysregulation of DNA methylation in differentiating monocytes, which affected several transcription regulators important for monocyte differentiation (e.g., <i>FLT3, HDAC1, MNT</i>) and led to enhanced generation of intermediate monocytes. As potential mediator, the uremic toxin and methylation inhibitor S-adenosylhomocysteine induced shifts in monocyte subsets <i>in vitro</i>, and associated with monocyte subset counts <i>in vivo</i>. Our data support the concept of monocyte trichotomy and the distinct role of intermediate monocytes in human immunity. The shift in monocyte subsets that occurs in chronic kidney disease, a proinflammatory condition of substantial epidemiological impact, may be induced by accumulation of uremic toxins that mediate epigenetic dysregulation.
DOI: 10.6084/m9.figshare.3125566
title: Evaluation of <i>Factor V Leiden, Prothrombin G20210A, MTHFR C677T</i> and <i>MTHFR A1298C</i> gene polymorphisms in retinopathy of prematurity in a Turkish cohort

description: <i>Background</i>: To assess <i>Factor V Leiden (FVL)</i> (rs6025), <i>Prothrombin G20210A</i> (rs1799963), <i>MTHFR C677T</i> (rs1801133), and <i>MTHFR A1298C</i> (rs1801131) gene mutations as risk factors in the development of retinopathy of prematurity (ROP). <i>Materials and methods</i>: A total of 105 children were included in this cross-sectional study. Patients were divided into two groups. The study group consisted of 55 infants with a history of ROP and the control group comprised 50 healthy infants with term birth. All subjects were screened for the presence of certain mutations (<i>FVL, Prothrombin G20210A, MTHFR C677T</i> and <i>MTHFR A1298C</i>) by Real-Time PCR at 1 year of age. <i>Results</i>: The mean gestational age (GA) and birth weight (BW) of the study group were, 28.65 ± 2.85 weeks and 1171 ± 385.74 g, respectively. There were no significant differences of genotype and allele frequency of <i>Prothrombin G20210A, MTHFR A1298C</i> and <i>MTHFR C677T</i> between the study and control groups (<i>p</i> &gt; 0.05). Eight children (14.5 %) had heterozygous and one child (1.8%) had homozygous <i>FVL</i> mutation in the study group. One child (2%) in the control group had heterozygous <i>FVL</i> mutation. There was statistically significant differences of <i>FVL</i> allele and genotype frequencies between the groups (<i>p</i> &lt; 0.05). <i>Conclusions</i>: The prevalence of <i>FVL</i> polymorphism (16.3 %) was higher in ROP patients than control subjects in this Turkish cohort. We suggest a possible association of <i>FVL</i> mutation with ROP at the end of the study.
DOI: 10.6084/m9.figshare.3125566.v1
title: Evaluation of <i>Factor V Leiden, Prothrombin G20210A, MTHFR C677T</i> and <i>MTHFR A1298C</i> gene polymorphisms in retinopathy of prematurity in a Turkish cohort

description: <i>Background</i>: To assess <i>Factor V Leiden (FVL)</i> (rs6025), <i>Prothrombin G20210A</i> (rs1799963), <i>MTHFR C677T</i> (rs1801133), and <i>MTHFR A1298C</i> (rs1801131) gene mutations as risk factors in the development of retinopathy of prematurity (ROP). <i>Materials and methods</i>: A total of 105 children were included in this cross-sectional study. Patients were divided into two groups. The study group consisted of 55 infants with a history of ROP and the control group comprised 50 healthy infants with term birth. All subjects were screened for the presence of certain mutations (<i>FVL, Prothrombin G20210A, MTHFR C677T</i> and <i>MTHFR A1298C</i>) by Real-Time PCR at 1 year of age. <i>Results</i>: The mean gestational age (GA) and birth weight (BW) of the study group were, 28.65 ± 2.85 weeks and 1171 ± 385.74 g, respectively. There were no significant differences of genotype and allele frequency of <i>Prothrombin G20210A, MTHFR A1298C</i> and <i>MTHFR C677T</i> between the study and control groups (<i>p</i> &gt; 0.05). Eight children (14.5 %) had heterozygous and one child (1.8%) had homozygous <i>FVL</i> mutation in the study group. One child (2%) in the control group had heterozygous <i>FVL</i> mutation. There was statistically significant differences of <i>FVL</i> allele and genotype frequencies between the groups (<i>p</i> &lt; 0.05). <i>Conclusions</i>: The prevalence of <i>FVL</i> polymorphism (16.3 %) was higher in ROP patients than control subjects in this Turkish cohort. We suggest a possible association of <i>FVL</i> mutation with ROP at the end of the study.
DOI: 10.6084/m9.figshare.3125362
title: DATASET_DREADDmice_videos.zip

description: context memory test
DOI: 10.6084/m9.figshare.3125599.v1
title: Розвідки на Житомирщині

description: Павленко С.В., Томашевський А.П., Борисов А.В., Переверзєв С.В. Розвідки на Житомирщині // Археологічні дослідження в Україні 2012. – К.: Волинські старожитності, 2013. – С. 156-157
DOI: 10.6084/m9.figshare.3125362.v1
title: DATASET_DREADDmice_videos.zip

description: context memory test
DOI: 10.6084/m9.figshare.3125236
title: Analytical representation of the density derivative of the Percus–Yevick hard-sphere radial distribution function

description: Explicit analytical expressions are presented for the density derivative, ∂<i>g</i><sub>HS</sub>(<i>R</i>; ρ)/∂ρ, of the Percus–Yevick approximation to the hard-sphere radial distribution function for <i>R</i> ≤ 6σ, where σ is the hard-sphere diameter and ρ = (<i>N</i>/<i>V</i>)σ<sup>3</sup> is the reduced density, where <i>N</i> is the number of particles and <i>V</i> is the volume. A FORTRAN program is provided for the implementation of these for <i>R</i> ≤ 6σ, which includes code for the calculation of <i>g</i><sub>HS</sub>(<i>R</i>; ρ) itself over this range. We also present and incorporate within the program code convenient analytical expressions for the numerical extrapolation of both quantities past <i>R</i> = 6σ. Our expressions are numerically tested against exact results.
DOI: 10.6084/m9.figshare.3125236.v1
title: Analytical representation of the density derivative of the Percus–Yevick hard-sphere radial distribution function

description: Explicit analytical expressions are presented for the density derivative, ∂<i>g</i><sub>HS</sub>(<i>R</i>; ρ)/∂ρ, of the Percus–Yevick approximation to the hard-sphere radial distribution function for <i>R</i> ≤ 6σ, where σ is the hard-sphere diameter and ρ = (<i>N</i>/<i>V</i>)σ<sup>3</sup> is the reduced density, where <i>N</i> is the number of particles and <i>V</i> is the volume. A FORTRAN program is provided for the implementation of these for <i>R</i> ≤ 6σ, which includes code for the calculation of <i>g</i><sub>HS</sub>(<i>R</i>; ρ) itself over this range. We also present and incorporate within the program code convenient analytical expressions for the numerical extrapolation of both quantities past <i>R</i> = 6σ. Our expressions are numerically tested against exact results.
DOI: 10.6084/m9.figshare.3125104
title: Metabolomic changes in murine serum following inhalation exposure to gasoline and diesel engine emissions

description: The adverse health effects of environmental exposure to gaseous and particulate components of vehicular emissions are a major concern among urban populations. A link has been established between respiratory exposure to vehicular emissions and the development of cardiovascular disease (CVD), but the mechanisms driving this interaction remain unknown. Chronic inhalation exposure to mixed vehicle emissions has been linked to CVD in animal models. This study evaluated the temporal effects of acute exposure to mixed vehicle emissions (MVE; mixed gasoline and diesel emissions) on potentially active metabolites in the serum of exposed mice. C57Bl/6 mice were exposed to a single 6-hour exposure to filtered air (FA) or MVE (100 or 300 μg/m<sup>3</sup>) by whole body inhalation. Immediately after and 18 hours after the end of the exposure period, animals were sacrificed for serum and tissue collection. Serum was analyzed for metabolites that were differentially present between treatment groups and time points. Changes in metabolite levels suggestive of increased oxidative stress (oxidized glutathione, cysteine disulfide, taurine), lipid peroxidation (13-HODE, 9-HODE), energy metabolism (lactate, glycerate, branched chain amino acid catabolites, butrylcarnitine, fatty acids), and inflammation (DiHOME, palmitoyl ethanolamide) were observed immediately after the end of exposure in the serum of animals exposed to MVE relative to those exposed to FA. By 18 hours post exposure, serum metabolite differences between animals exposed to MVE versus those exposed to FA were less pronounced. These findings highlight complex metabolomics alterations in the circulation following inhalation exposure to a common source of combustion emissions.