cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.8139317
title: Shareholder networks

description: This is the anonymised data defining two networks of shareholders, one for Turkey and one for The Netherlands. Each network describes the shareholdings in companies based in one country for the year 2014. An edge is present if two shareholders share an investment in the same company. The shareholders are also classified as being one of thirteen different types of owner. Full details are given in the paper https://arxiv.org/abs/1812.06694.
DOI: 10.6084/m9.figshare.8139317.v1
title: Shareholder network

description: This is the de-identified data for Shareholder Network, extracting from Amadeus, a company database of Bureau van Dijk (BvD). The authors' subscription of this database is provided by Imperial College London Library. (https://www.imperial.ac.uk/admin-services/library/subject-support/business/databases-a-z/) The authors download and proceed the data for Turkey and Netherlands, into edgelist files of edgelist and txt files of owner types. For detailed information please enquiry Bureau van Dijk (www.bvdinfo.com) The construction detail is available in the paper (https://arxiv.org/abs/1812.06694)
DOI: 10.6084/m9.figshare.8139317.v2
title: Shareholder networks

description: This is the anonymised data defining two networks of shareholders, one for Turkey and one for The Netherlands. Each network describes the shareholdings in companies based in one country for the year 2014. An edge is present if two shareholders share an investment in the same company. The shareholders are also classified as being one of thirteen different types of owner. Full details are given in the paper https://arxiv.org/abs/1812.06694.
DOI: 10.6084/m9.figshare.8139317.v4
title: Shareholder networks

description: This is the anonymised data defining two networks of shareholders, one for Turkey and one for The Netherlands. Each network describes the shareholdings in companies based in one country for the year 2014. An edge is present if two shareholders share an investment in the same company. The shareholders are also classified as being one of thirteen different types of owner. Full details are given in the paper https://arxiv.org/abs/1812.06694.
DOI: 10.6084/m9.figshare.8139317.v3
title: Shareholder networks

description: This is the anonymised data defining two networks of shareholders, one for Turkey and one for The Netherlands. Each network describes the shareholdings in companies based in one country for the year 2014. An edge is present if two shareholders share an investment in the same company. The shareholders are also classified as being one of thirteen different types of owner. Full details are given in the paper https://arxiv.org/abs/1812.06694.
DOI: 10.6084/m9.figshare.8139299
title: netherlands.edgelist

description: Edgelists for Netherlands shareholder network
DOI: 10.6084/m9.figshare.8139299.v2
title: netherlands.edgelist

description: Edgelists for Netherlands shareholder network
DOI: 10.6084/m9.figshare.8139299.v1
title: netherlands.edgelist

description: Edgelists for Netherlands shareholder network
DOI: 10.6084/m9.figshare.8139296
title: netherlands_id_ot.txt
DOI: 10.6084/m9.figshare.8139296.v2
title: netherlands_id_ot.txt

description: Node dictionary for Netherlands shareholder network
DOI: 10.6084/m9.figshare.8139296.v1
title: netherlands_id_ot.txt

description: Node dictionary for Netherlands shareholder network
DOI: 10.6084/m9.figshare.8139290
title: wqp_raw.zip

description: The five files contained in this compressed folder contain all water quality records downloaded from the Water Quality Portal on May 2nd, 2019. The five parameters are: Colored Dissolved Organic Matter (CDOM), Chlorophyll a (chlorophyll), Total Suspended Solids (TSS), Dissolved Organic Carbon (DOC), and Secchi Disk Depth (secchi). These data cover the continental united states and Alaska. These are raw outputs and just aggregated, all metadata are available here: https://www.waterqualitydata.us/. <br><br>This data was part of building the AquaSat dataset with a github repo here: https://github.com/GlobalHydrologyLab/watersat <br><br>And a paper DOI here: <br>
DOI: 10.5281/zenodo.3549602
title: Agile Success Model

description: Preliminary version
DOI: 10.6084/m9.figshare.8139281
title: <i>In vivo</i> study of mPEG–PCL as a nanocarriers for anti-inflammatory drug delivery of simvastatin

description: <b>Purpose:</b> In this study, methoxy poly (ethylene glycol)-poly (ε-caprolactone) (mPEG–PCL) di-block copolymers were synthesized. The purpose of this work is to investigate the <i>in vivo</i> anti-inflammatory effects of simvastatin-loaded micelles. <b>Methods</b>: The structure of synthesized copolymers was characterized by using HNMR, FTIR, and GPC techniques. Simvastatin was encapsulated in micelles through a single-step nano-precipitation method, leading to the formation of simvastatin-loaded mPEG–PCL (simvastatin-mPEG–PCL) micelles. In this study, the anti-inflammatory effects of simvastatin/mPEG–PCL micelles versus indomethacin were investigated in acute inflammation-induced rats. The paw edema thickness was measured 1, 2, 3, and 4 h after injection of formulation. The inhibition of edema in various groups were calculated and reported by percentages. <b>Results:</b> The results showed that the zeta potential of micelles was about −14.9 ± 0.47 mV and the average size was in range of 66.10 ± 0.34 nm. Simvastatin was encapsulated in mPEG–PCL micelles with a loading capacity of 9.63 ± 0.87% and an encapsulation efficiency of 64.20 ± 0.79%. Simvastatin and simvastatin-mPEG–PCL micelles showed significant anti-inflammatory activity in the present study. <b>Conclusions:</b> This study revealed that simvastatin and simvastatin/mPEG–PCL micelles both have anti-inflammatory effects and suggested that statins have potential anti-inflammatory activity along with their lipid lowering properties.
DOI: 10.6084/m9.figshare.8139281.v1
title: <i>In vivo</i> study of mPEG–PCL as a nanocarriers for anti-inflammatory drug delivery of simvastatin

description: <b>Purpose:</b> In this study, methoxy poly (ethylene glycol)-poly (ε-caprolactone) (mPEG–PCL) di-block copolymers were synthesized. The purpose of this work is to investigate the <i>in vivo</i> anti-inflammatory effects of simvastatin-loaded micelles. <b>Methods</b>: The structure of synthesized copolymers was characterized by using HNMR, FTIR, and GPC techniques. Simvastatin was encapsulated in micelles through a single-step nano-precipitation method, leading to the formation of simvastatin-loaded mPEG–PCL (simvastatin-mPEG–PCL) micelles. In this study, the anti-inflammatory effects of simvastatin/mPEG–PCL micelles versus indomethacin were investigated in acute inflammation-induced rats. The paw edema thickness was measured 1, 2, 3, and 4 h after injection of formulation. The inhibition of edema in various groups were calculated and reported by percentages. <b>Results:</b> The results showed that the zeta potential of micelles was about −14.9 ± 0.47 mV and the average size was in range of 66.10 ± 0.34 nm. Simvastatin was encapsulated in mPEG–PCL micelles with a loading capacity of 9.63 ± 0.87% and an encapsulation efficiency of 64.20 ± 0.79%. Simvastatin and simvastatin-mPEG–PCL micelles showed significant anti-inflammatory activity in the present study. <b>Conclusions:</b> This study revealed that simvastatin and simvastatin/mPEG–PCL micelles both have anti-inflammatory effects and suggested that statins have potential anti-inflammatory activity along with their lipid lowering properties.
DOI: 10.6084/m9.figshare.8139227
title: turkey.edgelist

description: The edgelist of Turkey shareholder network
DOI: 10.6084/m9.figshare.8139227.v2
title: turkey.edgelist

description: The edgelist of Turkey shareholder network
DOI: 10.6084/m9.figshare.8139227.v1
title: turkey.edgelist

description: The edgelist of Turkey shareholder network
DOI: 10.6084/m9.figshare.8139224
title: turkey_id_ot.txt

description: This is the owner type dictionary of Turkey shareholder network.
DOI: 10.6084/m9.figshare.8139224.v2
title: turkey_id_ot.txt

description: This is the owner type dictionary of Turkey shareholder network.
DOI: 10.6084/m9.figshare.8139224.v1
title: turkey_id_ot.txt

description: This is the owner type dictionary of Turkey shareholder network.
DOI: 10.6084/m9.figshare.8139203
title: Supplementary Material for: Atopic Patients Show Increased Interleukin 4 Plasma Levels but the Degree of Elevation Is Not Sufficient to Upregulate Interleukin-4-Sensitive Genes

description: <b><i>Background:</i></b> Atopic diseases constitute a major health challenge for industrialized countries, and elevated levels of interleukin 4 (IL-4) frequently characterize these disorders. Previous in vitro<i></i>analyses have indicated that IL-4 strongly upregulates the expression of IL-4-sensitive genes in human monocytes. <b><i>Objective:</i></b> To explore whether similar expression alterations may contribute to the pathomechanisms of atopic diseases in vivo we carried out a small-scale case-control clinical study (<i>n</i> = 43), in which we quantified the plasma levels of IgE and IL-4 as well as the expression of selected IL-4-sensitive genes in blood leukocytes. <b><i>Methods:</i></b> 34 allergic patients suffering from allergic rhinitis (<i>n</i> = 11), atopic eczema (<i>n</i> = 11) and allergic asthma (<i>n</i> = 12) as well as 9 healthy control individuals were recruited. IgE and IL-4 plasma levels were determined by ELISA, and the expression of selected IL-4-sensitive gene products in blood leukocytes was quantified by qRT-PCR. In addition, the fatty acid oxygenase activity of isolated monocytes was measured by RP-HPLC analysis of the arachidonic acid oxygenation products (ex vivo activity assays). <b><i>Results:</i></b> We found that plasma levels of IgE and IL-4 were significantly elevated in atopic patients but the degree of elevation was not sufficient to upregulate the expression of the selected IL-4-sensitive genes in circulating leukocytes. Moreover, the arachidonic acid oxygenase activity of blood monocytes was not significantly altered in atopic patients. <b><i>Conclusion:</i></b> Our data suggest that the IL-4 plasma levels of atopic patients are not high enough to impact the expression of IL-4-sensitive genes.
DOI: 10.6084/m9.figshare.8139188
title: Supplementary appendix

description: Supplementary Appendix_Stamou et al_2019
DOI: 10.6084/m9.figshare.8139188.v1
title: Supplementary appendix

description: Supplementary Appendix_Stamou et al_2019
DOI: 10.6084/m9.figshare.8139113
title: Supplementary Material for: Low-Intensity Exercise Suppresses CCAAT/Enhancer-Binding Protein δ/Myostatin Pathway Through Androgen Receptor in Muscle Cells

description: <b><i>Background:</i></b> Androgen production following exercise has been suggested to contribute anabolic actions of muscle. However, the underlying mechanisms of the androgen receptor (AR) in androgen’s action are still unclear. <b><i>Objective:</i></b> In the present study, we examined androgen/AR-mediated action in exercise, especially for the suppression of myostatin, a potent negative regulator of muscle mass. <b><i>Methods:</i></b> To examine the effects of exercise, we employed low-intensity exercise in mice and electric pulse stimulation (EPS) in C2C12 myotubes. Androgen production by C2C12 myotubes was measured by enzyme-linked immunosorbent assay. To block the action of AR, we pretreated C2C12 myotubes with flutamide. Quantitative real-time polymerase chain reaction was used to determine the expression levels of proteolytic genes including CCAAT/enhancer-binding protein delta (C/EBPδ), myostatin and muscle E3 ubiquitin ligases, as well as myogenic genes such as myogenin and PGC1α. The activation of 5′-adenosine-activated protein kinase and STAT3 was determined by Western blot analysis. <b><i>Results:</i></b> Both mRNA and protein levels of AR significantly increased in skeletal muscle of low-intensity exercised mice and C2C12 myotubes exposed to EPS. Production of testosterone and dihydrotestosterone from EPS-treated C2C12 myotubes was markedly increased. Of interest, we found that myostatin was clearly inhibited by EPS, and its inhibition was significantly abrogated when AR was blocked by flutamide. To test how AR suppresses myostatin, we examined the effects of EPS on C/EBPδ because the promoter region of myostatin has several C/EBP recognition sites. C/EBPδ expression was decreased by EPS, and this decrease was negated by flutamide. IL-6 and phospho-STAT3 (pSTAT3) expression, the downstream pathway of myostatin, were decreased by EPS and this was also reversed by flutamide. Similar downregulation of C/EBPδ, myostatin, and IL-6 was seen in skeletal muscle of low-intensity exercised mice. <b><i>Conclusions:</i></b> Muscle AR expression and androgen production were increased by exercise and EPS treatment. As a mechanistical insight, it is suggested that AR inhibited myostatin expression transcriptionally by C/EBPδ suppression, which negatively influences IL-6/pSTAT3 expression and consequently contributes to the prevention of muscle proteolysis during exercise.
DOI: 10.5281/zenodo.3997305
title: HRM practices and turnover intentions.

description: Data Set
DOI: 10.5281/zenodo.3997304
title: HRM practices and turnover intentions.

description: Data Set
DOI: 10.6084/m9.figshare.8138828
title: Supplementary Material for: Importance of Genetic Diagnostics in Adult-Onset Focal Segmental Glomerulosclerosis

description: Focal segmental glomerulosclerosis (FSGS) is a histological pattern of podocyte and glomerulus injury. FSGS can be primary and secondary to other diseases or due to a genetic cause. Strikingly, genetic causes for adult-onset FSGS are often overlooked, likely because identifying patients with genetic forms of FSGS based on clinical presentation and histopathology is difficult. Yet diagnosing genetic FSGS does not only have implications for prognostication and therapy but also for family and family planning. In this case series, we present 3 adult patients who presented with advanced renal disease with the histological picture of FSGS and proved to have a genetic cause of the disease, namely, variants in <i>INF2</i>, <i>COL4A4</i> and <i>HNF1B</i>, respectively. We show the possibilities of identifying genetic FSGS based on clinical clues of a positive family history, early age at onset of disease, and/or severe therapy-resistant disease. We discuss ways to select the method of genetic testing for individual patients. Finally, we examine how the judicious use of genetic investigations can obviate potential harmful diagnostic procedures and direct clinical decisions in patients and their relatives.
DOI: 10.6084/m9.figshare.8138828.v1
title: Supplementary Material for: Importance of Genetic Diagnostics in Adult-Onset Focal Segmental Glomerulosclerosis

description: Focal segmental glomerulosclerosis (FSGS) is a histological pattern of podocyte and glomerulus injury. FSGS can be primary and secondary to other diseases or due to a genetic cause. Strikingly, genetic causes for adult-onset FSGS are often overlooked, likely because identifying patients with genetic forms of FSGS based on clinical presentation and histopathology is difficult. Yet diagnosing genetic FSGS does not only have implications for prognostication and therapy but also for family and family planning. In this case series, we present 3 adult patients who presented with advanced renal disease with the histological picture of FSGS and proved to have a genetic cause of the disease, namely, variants in <i>INF2</i>, <i>COL4A4</i> and <i>HNF1B</i>, respectively. We show the possibilities of identifying genetic FSGS based on clinical clues of a positive family history, early age at onset of disease, and/or severe therapy-resistant disease. We discuss ways to select the method of genetic testing for individual patients. Finally, we examine how the judicious use of genetic investigations can obviate potential harmful diagnostic procedures and direct clinical decisions in patients and their relatives.
DOI: 10.6084/m9.figshare.8138792
title: Milky Way globular clusters in gamma-rays

description: Data generated from the paper De Menezes, Cafardo & Nemmen 2019, "Milky Way globular clusters in gamma-rays: analysing the dynamical formation of millisecond pulsars" published in MNRAS (DOI 10.1093/mnras/stz898). This dataset includes the following files:<br>1. all figures from the paper (`figures.zip`)2. results of spectral fits to the globular clusters Fermi LAT emission (`spectral-fits.zip`)3. FITS files with the TS maps for all sources (`ts-maps.zip`)<br>More information about each of the data products above are included below. This text is also included in the file `README.md` included. <br># 1. Figures from paper<br>All the plots included in the latest version of the paper are included in file `figures.zip` in the PNG format.<br># 2. Spectral fits to the globular clusters *Fermi* LAT emission <br>The file `spectral-fits.zip` includes ASCII files with the output from the spectral fits performed to each of the 157 globular clusters analysed, such as <br>- flux- spectrum type- prefactor - index<br>The modelling was carried out with FermiPy v0.16.0.<br># 3. FITS files with the TS maps for all sources <br>The file `ts-maps.zip` includes FITS files with the images for the TS maps generated for the field of each globular cluster. <br>The value of TS corresponds roughly to the square of the statistical significance of the presence of a point source above background, in standard deviations. As such, a value of TS=25 would correspond to a source detected at ~5sigma.<br>
DOI: 10.6084/m9.figshare.8138792.v1
title: Milky Way globular clusters in gamma-rays

description: Data generated from the paper De Menezes, Cafardo & Nemmen 2019, "Milky Way globular clusters in gamma-rays: analysing the dynamical formation of millisecond pulsars" published in MNRAS (DOI 10.1093/mnras/stz898). This dataset includes the following files:<br>1. all figures from the paper (`figures.zip`)2. results of spectral fits to the globular clusters Fermi LAT emission (`spectral-fits.zip`)3. FITS files with the TS maps for all sources (`ts-maps.zip`)<br>More information about each of the data products above are included below. This text is also included in the file `README.md` included. <br># 1. Figures from paper<br>All the plots included in the latest version of the paper are included in file `figures.zip` in the PNG format.<br># 2. Spectral fits to the globular clusters *Fermi* LAT emission <br>The file `spectral-fits.zip` includes ASCII files with the output from the spectral fits performed to each of the 157 globular clusters analysed, such as <br>- flux- spectrum type- prefactor - index<br>The modelling was carried out with FermiPy v0.16.0.<br># 3. FITS files with the TS maps for all sources <br>The file `ts-maps.zip` includes FITS files with the images for the TS maps generated for the field of each globular cluster. <br>The value of TS corresponds roughly to the square of the statistical significance of the presence of a point source above background, in standard deviations. As such, a value of TS=25 would correspond to a source detected at ~5sigma.<br>
DOI: 10.6084/m9.figshare.8138669
title: Residue Enzyme Activity.xlsx

description: Residue enzyme activity data
DOI: 10.6084/m9.figshare.8138669.v1
title: Residue Enzyme Activity.xlsx

description: Residue enzyme activity data
DOI: 10.6084/m9.figshare.8138573
title: Result of CICA-MO(mutation rate=0.5)

description: The datasets for the results of CICA-MO with muation rate of 0.5 to solve the path planning problem. Including the result table and the metadata.
DOI: 10.6084/m9.figshare.8138573.v1
title: Result of CICA-MO(mutation rate=0.5)

description: The datasets for the results of CICA-MO with muation rate of 0.5 to solve the path planning problem. Including the result table and the metadata.
DOI: 10.6084/m9.figshare.8138471
title: Computational approach identifies protein off-targets for Isoniazid-NAD adduct: hypothesizing a possible drug resistance mechanism in <i>Mycobacterium tuberculosis</i>

description: Isoniazid is an important antitubercular molecule identified as a drug of choice in tuberculosis treatment. As such, INH is an inactive prodrug; it acquires an active conformation by forming an adduct with NAD. The adduct targets inhA protein, a reductase responsible for fatty acid chain elongation in the cell wall of <i>Mycobacterium tuberculosis</i>. Resistance to INH is majorly contributed by mutations in <i>inhA, katG</i> and geneic and non-geneic regions associated with efflux genes. Despite being widespread, the mechanism of resistance remains unknown in ∼15% of INH-resistant strains. Studies report that an intracellular increase in NADH concentration prevents inhA inhibition, leading to INH resistance. In the pursuit of finding possible resistance mechanisms, we set out to find NAD binding proteins to explore similarities in structure and NAD binding property of these proteins with that of inhA. We identified 172 NAD binding proteins, of which 53 were identified to have sequence or structural similarity to inhA. By performing docking analysis on selected proteins, we identified INH-adduct to have good binding affinity despite very minimal structural similarity to inhA. This analysis was further supported by principal component analysis, which identified 65 proteins with NAD binding conformation similar to that of inhA. These findings prompt us to hypothesize that upon exposure to INH, bacteria tries to reduce inhA susceptibility by inducing expression of these NAD binding proteins through increase in NADH concentration. This in turn favours off-target binding and leads to decreased binding and potency of INH, thus contributing indirectly to INH resistance. Communicated by Ramaswamy H. Sarma
DOI: 10.6084/m9.figshare.8138471.v2
title: Computational approach identifies protein off-targets for Isoniazid-NAD adduct: hypothesizing a possible drug resistance mechanism in <i>Mycobacterium tuberculosis</i>

description: Isoniazid is an important antitubercular molecule identified as a drug of choice in tuberculosis treatment. As such, INH is an inactive prodrug; it acquires an active conformation by forming an adduct with NAD. The adduct targets inhA protein, a reductase responsible for fatty acid chain elongation in the cell wall of <i>Mycobacterium tuberculosis</i>. Resistance to INH is majorly contributed by mutations in <i>inhA, katG</i> and geneic and non-geneic regions associated with efflux genes. Despite being widespread, the mechanism of resistance remains unknown in ∼15% of INH-resistant strains. Studies report that an intracellular increase in NADH concentration prevents inhA inhibition, leading to INH resistance. In the pursuit of finding possible resistance mechanisms, we set out to find NAD binding proteins to explore similarities in structure and NAD binding property of these proteins with that of inhA. We identified 172 NAD binding proteins, of which 53 were identified to have sequence or structural similarity to inhA. By performing docking analysis on selected proteins, we identified INH-adduct to have good binding affinity despite very minimal structural similarity to inhA. This analysis was further supported by principal component analysis, which identified 65 proteins with NAD binding conformation similar to that of inhA. These findings prompt us to hypothesize that upon exposure to INH, bacteria tries to reduce inhA susceptibility by inducing expression of these NAD binding proteins through increase in NADH concentration. This in turn favours off-target binding and leads to decreased binding and potency of INH, thus contributing indirectly to INH resistance. Communicated by Ramaswamy H. Sarma