cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1452976
title: Spatio-Temporal Network Visualisations

description: Visualisations of the time-varying connectivity of spatio-temporal networks. <strong>Networks</strong> <em><strong>C. Elegans</strong></em>: Cellular nervous system of the roundworm caenorhabditis elegans. <strong>StudentLife</strong>: Mobile communication (SMS and phone calls) among a cohort of Dartmouth College students participating in the StudentLife experiment. <strong>Underground</strong>: The London Underground rapid transit system.<strong>Paris</strong>: The Paris Metro rapid transit system.<strong>New York</strong>: The New York City Subway rapid transit system. <strong>Flights</strong>: The US domestic flights network. <strong>Format</strong> MPEG-4 (mp4) movie file. No audio. <strong>Additional information</strong> The datasets used to generate these visualisations are available on Dryad: http://dx.doi.org/10.5061/dryad.3p27r Further description of the data is available here:<br>http://mattjw.net/pub/stnetsIf you find these visualisations or data useful, please reference the counterpart scientific article: <br>Williams M.J., Musolesi M. (2016) "Spatio-temporal networks: reachability, centrality, and robustness", Royal Society Open Science
DOI: 10.6084/m9.figshare.1452993.v1
title: Voxelwise Maps to Accompany Fox et al., 2015 PNAS

description: Voxelwise Maps to Accompany Fox et al., 2015 PNAS The enclosed .tar.gz file contains voxelwise statistical maps of anxious temperament related metabolism and brian volume, as well as heritability estimates for these measures to acompany Fox AS, et al. (2015)<em>. </em> Specifically, it contains: 1) MRI Template: template_meanT1_n592.nii 2) Anixous Temperament related metabolism t-map: FoxEtAl_PNAS_2015_AT_FDGPET_t.nii 3) Anixous Temperament related log jacobian t-map: FoxEtAl_PNAS_2015_AT_LogJacobian_t.nii 4) Heritability of FDG-PET, h^2- and p-maps: FoxEtAl_PNAS_2015_FDGPET_h2.nii FoxEtAl_PNAS_2015_FDGPET_h2_p.nii 5) Heritability of log jacobian determinant, h^2- and p-maps: FoxEtAl_PNAS_2015_LogJacobian_h2.nii FoxEtAl_PNAS_2015_LogJacobian_h2_p.nii Additional information can be found in: Fox AS, Oler JA, Shackman AJ, Shelton SE, Raveendran M, McKay DR, Converse AK, Alexander AL, Davidson RJ, Blangero J, Rogers J, & Kalin NH (2015). Intergenerational neural mediators of early-life anxious temperament.<em> Proceedings of the National Academy of Sciences.</em> In Press.
DOI: 10.6084/m9.figshare.1453169.v6
title: A visual dataset of dance steps for behavioral experimentation.

description: A database of short video clips of dance steps with a number of manipulations (e.g., dance step with or without arm movements, slow or fast executions of the same step). The clips are visual only and have been used in research previously (e.g., Sgouramani & Vatakis,<br>2014).
DOI: 10.6084/m9.figshare.1452960
title: Fileset S1, S2, S3, S4

description: Conjunto de quatro suplementos (S1, S2, S3, S4) citados no artigo publicado na revista rodriguésia ("Vegetação endêmica e espécie invasora em campos rupestres de áreas garimpadas").
DOI: 10.6084/m9.figshare.1452969
title: University of Luxembourg | PhD records without on-line PhD thesis publications | @ 18/6/2015

description: Via Open Repository and Bibliography Luxembourg (ORBi lu).
DOI: 10.17632/ptd9fnsrtr.1
title: Prominent Binary-Feature (Permissions) Frequencies for Android Mobile Benign Apps and Malware Datasets

description: The following academic datasets provided the frequencies of prominent binary-features, namely Android application permission requests* for the negative and positive classes. They are used in analyzing the dataset dissimilarities via the method proposed by Gürol Canbek. Negative/Positive dataset pairs** and their references - DS0 by (Lindorfer et al., 2014). (ANDRUBIS) as it is called "Touchstone Dataset" in the related article - DS1 by (Aswini and Vinod, 2014). (Contagio) - DS2 by (Wang et al., 2014)*** - DS3 by (Yerima et al., 2014)*** - DS4 by (Jiang and Zhou, 2013). (Android Malware Genome Project, AMGP) - DS5 (Peng et al., 2012) Thanks to the authors providing the data. * https://developer.android.com/reference/android/Manifest.permission.html ** DS4 is a positive-class only dataset (it does not negative-class samples) *** DS2 and DS3 positive-class datasets contain DS4 (AMGP) samples.
DOI: 10.6084/m9.figshare.1452960.v1
title: Fileset S1, S2, S3, S4

description: Conjunto de quatro suplementos (S1, S2, S3, S4) citados no artigo publicado na revista rodriguésia ("Vegetação endêmica e espécie invasora em campos rupestres de áreas garimpadas").
DOI: 10.6084/m9.figshare.1452948
title: Spatio-Temporal Public Transport Networks

description: <strong>Overview</strong> Datasets describing the time-varying properties of spatially embedded public transport networks. <strong>Networks</strong> Four public transport networks are provided. <em><strong>London Underground</strong></em>: Timetabled London Underground journeys for two days. Specifically, 2015-02-09 00:00 to 2015-02-11 00:00 (GMT).<em><strong>Paris Metro</strong></em>: Timetabled Paris Metro journeys for two days. Specifically, 2015-11-30 00:00 to 2015-12-02 00:00 (CET).<em><strong>New York Subway</strong></em>: Timetabled New York Subway journeys for two days. Specifically, 2015-11-30 00:00 to 2015-12-02 00:00 (EST). <em><strong>US Domestic Flights</strong></em>: Actual flights among 299 US airports over 10 days. Specifically, 2014-02-03 00:00 to 2014-02-13 00:00 (EST). This is derived from the Airline On-Time Performance data collected by the US Bureau of Transportation Statistics. <strong>Format</strong> Each dataset consits of two files. The "network" CSV file (*_stnet.csv.gz) describes the time-evolution of the network's topology. This includes the time-varying transit speed between two stations. This file is in the LMF Aggregate Format, a non-proprietary format for multiplex networks. The "coordinates" CSV file (*_coords.csv.gz) provides the geographic locations of each node. <strong>Additional information</strong> Additional detail specific to these transport networks is available here: http://mattjw.net/pub/stnets/
DOI: 10.6084/m9.figshare.1452969.v1
title: University of Luxembourg | PhD theses without on-line PhD thesis publications | @ 18/6/2015

description: Via Open Repository and Bibliography Luxembourg (ORBi lu)
DOI: 10.6084/m9.figshare.1452914
title: <i>Drosophila</i> Gyf/GRB10 interacting GYF protein is an autophagy regulator that controls neuron and muscle homeostasis

description: Autophagy is an essential process for eliminating ubiquitinated protein aggregates and dysfunctional organelles. Defective autophagy is associated with various degenerative diseases such as Parkinson disease. Through a genetic screening in <i>Drosophila</i>, we identified <i>CG11148</i>, whose product is orthologous to GIGYF1 (GRB10-interacting GYF protein 1) and GIGYF2 in mammals, as a new autophagy regulator; we hereafter refer to this gene as <i>Gyf</i>. Silencing of <i>Gyf</i> completely suppressed the effect of Atg1-Atg13 activation in stimulating autophagic flux and inducing autophagic eye degeneration. Although <i>Gyf</i> silencing did not affect Atg1-induced Atg13 phosphorylation or Atg6-Pi3K59F (class III PtdIns3K)-dependent Fyve puncta formation, it inhibited formation of Atg13 puncta, suggesting that Gyf controls autophagy through regulating subcellular localization of the Atg1-Atg13 complex. <i>Gyf</i> silencing also inhibited Atg1-Atg13-induced formation of Atg9 puncta, which is accumulated upon active membrane trafficking into autophagosomes. <i>Gyf</i>-null mutants also exhibited substantial defects in developmental or starvation-induced accumulation of autophagosomes and autolysosomes in the larval fat body. Furthermore, heads and thoraxes from <i>Gyf</i>-null adults exhibited strongly reduced expression of autophagosome-associated Atg8a-II compared to wild-type (WT) tissues. The decrease in Atg8a-II was directly correlated with an increased accumulation of ubiquitinated proteins and dysfunctional mitochondria in neuron and muscle, which together led to severe locomotor defects and early mortality. These results suggest that Gyf-mediated autophagy regulation is important for maintaining neuromuscular homeostasis and preventing degenerative pathologies of the tissues. Since human mutations in the <i>GIGYF2</i> locus were reported to be associated with a type of familial Parkinson disease, the homeostatic role of Gyf-family proteins is likely to be evolutionarily conserved.
DOI: 10.17632/9bf53dvvp7.1
title: Mood-related behavioral and neurochemical alterations in mice exposed to low chlorpyrifos levels during the brain growth spurt.

description: We hypothesize that the brain growth spurt is a critical period concerning CPF-induced mood-related alterations on brain function, and that neurochemical and behavioral alterations would be identified even after a CPF dose that evokes negligible levels of AChE inhibition. To verify this hypothesis, we exposed neonatal mice to a subchronic low-level regimen of CPF exposure that did not result in a significant inhibition of AChE activity in the brain. We evaluated the effects CPF on mood using a battery of behavioral tests: open field, elevated plus maze and forced swimming tests. Considering the relevant association among the cholinergic system, the serotonergic system and mood disorders, we evaluated these two neurotransmitter systems in the cerebral cortex and brainstem both by the end of exposure and at adulthood. Regarding the cholinergic system, we assessed the binding of [3H] hemicholinium-3 (HC-3) to the high-affinity presynaptic choline transporter (Ch transporter) and the choline acetyltransferase (ChAT) activity. As for serotonergic system, we choose to assess 5-HT1A and 5-HT2 receptors, and the presynaptic 5-HT transporter.
DOI: 10.6084/m9.figshare.1452969.v2
title: (being updated) University of Luxembourg | PhD theses without on-line PhD thesis publications | @ 18/6/2015

description: (being updated) Via Open Repository and Bibliography Luxembourg (ORBi lu)
DOI: 10.6084/m9.figshare.1452914.v1
title: <i>Drosophila</i> Gyf/GRB10 interacting GYF protein is an autophagy regulator that controls neuron and muscle homeostasis

description: Autophagy is a process essential for eliminating ubiquitinated protein aggregates and dysfunctional organelles. Defective autophagy is associated with various degenerative diseases such as Parkinson disease. Through a genetic screening in <i>Drosophila</i>, we identified <i>CG11148</i>, whose product is orthologous to GIGYF1 (GRB10 interacting GYF protein 1) and GIGYF2 in mammals, as a new autophagy regulator; we hereafter refer to this gene as <i>Gyf</i>. Silencing of <i>Gyf</i> completely suppressed the effect of Atg1-Atg13 activation in stimulating autophagic flux and inducing autophagic eye degeneration. Although <i>Gyf</i> silencing did not affect Atg1-induced Atg13 phosphorylation or Atg6-Pi3K59F (class III PtdIns3K)-dependent Fyve puncta formation, it inhibited formation of Atg13 puncta, suggesting that Gyf controls autophagy through regulating subcellular localization of the Atg1-Atg13 complex. <i>Gyf</i> silencing also inhibited Atg1-Atg13-induced formation of Atg9 puncta, which is accumulated upon active membrane trafficking into autophagosomes. <i>Gyf</i>-null mutants also exhibited substantial defects in developmental or starvation-induced accumulation of autophagosomes and autolysosomes in the larval fat body. Furthermore, heads and thoraxes from <i>Gyf</i>-null adults exhibited strongly reduced expression of autophagosome-associated Atg8a-II compared to wild-type (WT) tissues. The decrease in Atg8a-II was directly correlated with an increased accumulation of ubiquitinated proteins and dysfunctional mitochondria in neuron and muscle, which together led to severe locomotor defects and early mortality. These results suggest that Gyf-mediated autophagy regulation is important for maintaining neuromuscular homeostasis and preventing degenerative pathologies of the tissues. Since human mutations in the <i>GIGYF2</i> locus were reported to be associated with a type of familial Parkinson disease, the homeostatic role of Gyf-family proteins is likely to be evolutionarily conserved.
DOI: 10.6084/m9.figshare.1452969.v3
title: (being updated) University of Luxembourg | PhD theses without on-line PhD thesis publications | @ 18/6/2015

description: (being updated) Via Open Repository and Bibliography Luxembourg (ORBi lu)
DOI: 10.17632/8nxk8f36j7.3
title: DED melt pool dimensions ANN dataset

description: Melt pool dimensions of cross-sections of single track DED deposits produced by a Trumpf TruLaser Cell 7040. More details of the work herein are contained in the work titled "On the use of Artificial Neural Networks to Determine Processing Windows in Directed Energy Deposition Applications".
DOI: 10.6084/m9.figshare.1452913.v1
title: Export-deficient monoubiquitinated PEX5 triggers peroxisome removal in SV40 large T antigen-transformed mouse embryonic fibroblasts

description: Peroxisomes are ubiquitous cell organelles essential for human health. To maintain a healthy cellular environment, dysfunctional and superfluous peroxisomes need to be selectively removed. Although emerging evidence suggests that peroxisomes are mainly degraded by pexophagy, little is known about the triggers and molecular mechanisms underlying this process in mammalian cells. In this study, we show that PEX5 proteins fused to a bulky C-terminal tag trigger peroxisome degradation in SV40 large T antigen-transformed mouse embryonic fibroblasts. In addition, we provide evidence that this process is autophagy-dependent and requires monoubiquitination of the N-terminal cysteine residue that marks PEX5 for recycling. As our findings also demonstrate that the addition of a bulky tag to the C terminus of PEX5 does not interfere with PEX5 monoubiquitination but strongly inhibits its export from the peroxisomal membrane, we hypothesize that such a tag mimics a cargo protein that cannot be released from PEX5, thus keeping monoubiquitinated PEX5 at the membrane for a sufficiently long time to be recognized by the autophagic machinery. This in turn suggests that monoubiquitination of the N-terminal cysteine of peroxisome-associated PEX5 not only functions to recycle the peroxin back to the cytosol, but also serves as a quality control mechanism to eliminate peroxisomes with a defective protein import machinery.
DOI: 10.6084/m9.figshare.1452908
title: Sexual dimorphism in conspicuousness and ornamentation in an enigmatic lizard from Sri Lanka, the leaf-nosed lizard Ceratophora tennentii

description: This is the entire bitbucket git repository that contains the necessary data, code, figures, tables etc for paper. If just interested in the data itself please just see "Final_Data_Files" within the "Data" folder. The "SpecData.csv" contains the processed spec files for the labial, throat and mouth areas. These were converted from a list to a dataframe in R and so areas need to be subsetted by id. column. All individual ID's are listed as column names and reflectance values are given for wavelengths between 300-700nm. "PerformMorph_data.csv" contains bite force and morphology data for all individuals which we had complete data for. "Morph_data.csv" contains all morphological data on all inidviduals for both sexes.
DOI: 10.6084/m9.figshare.1452914.v2
title: <i>Drosophila</i> Gyf/GRB10 interacting GYF protein is an autophagy regulator that controls neuron and muscle homeostasis

description: Autophagy is an essential process for eliminating ubiquitinated protein aggregates and dysfunctional organelles. Defective autophagy is associated with various degenerative diseases such as Parkinson disease. Through a genetic screening in <i>Drosophila</i>, we identified <i>CG11148</i>, whose product is orthologous to GIGYF1 (GRB10-interacting GYF protein 1) and GIGYF2 in mammals, as a new autophagy regulator; we hereafter refer to this gene as <i>Gyf</i>. Silencing of <i>Gyf</i> completely suppressed the effect of Atg1-Atg13 activation in stimulating autophagic flux and inducing autophagic eye degeneration. Although <i>Gyf</i> silencing did not affect Atg1-induced Atg13 phosphorylation or Atg6-Pi3K59F (class III PtdIns3K)-dependent Fyve puncta formation, it inhibited formation of Atg13 puncta, suggesting that Gyf controls autophagy through regulating subcellular localization of the Atg1-Atg13 complex. <i>Gyf</i> silencing also inhibited Atg1-Atg13-induced formation of Atg9 puncta, which is accumulated upon active membrane trafficking into autophagosomes. <i>Gyf</i>-null mutants also exhibited substantial defects in developmental or starvation-induced accumulation of autophagosomes and autolysosomes in the larval fat body. Furthermore, heads and thoraxes from <i>Gyf</i>-null adults exhibited strongly reduced expression of autophagosome-associated Atg8a-II compared to wild-type (WT) tissues. The decrease in Atg8a-II was directly correlated with an increased accumulation of ubiquitinated proteins and dysfunctional mitochondria in neuron and muscle, which together led to severe locomotor defects and early mortality. These results suggest that Gyf-mediated autophagy regulation is important for maintaining neuromuscular homeostasis and preventing degenerative pathologies of the tissues. Since human mutations in the <i>GIGYF2</i> locus were reported to be associated with a type of familial Parkinson disease, the homeostatic role of Gyf-family proteins is likely to be evolutionarily conserved.
DOI: 10.6084/m9.figshare.1452969.v4
title: (being updated) University of Luxembourg | PhD theses without on-line PhD thesis publications | @ 18/6/2015

description: (being updated) Via Open Repository and Bibliography Luxembourg (ORBi lu)
DOI: 10.6084/m9.figshare.1452913.v2
title: Export-deficient monoubiquitinated PEX5 triggers peroxisome removal in SV40 large T antigen-transformed mouse embryonic fibroblasts

description: Peroxisomes are ubiquitous cell organelles essential for human health. To maintain a healthy cellular environment, dysfunctional and superfluous peroxisomes need to be selectively removed. Although emerging evidence suggests that peroxisomes are mainly degraded by pexophagy, little is known about the triggers and molecular mechanisms underlying this process in mammalian cells. In this study, we show that PEX5 proteins fused to a bulky C-terminal tag trigger peroxisome degradation in SV40 large T antigen-transformed mouse embryonic fibroblasts. In addition, we provide evidence that this process is autophagy-dependent and requires monoubiquitination of the N-terminal cysteine residue that marks PEX5 for recycling. As our findings also demonstrate that the addition of a bulky tag to the C terminus of PEX5 does not interfere with PEX5 monoubiquitination but strongly inhibits its export from the peroxisomal membrane, we hypothesize that such a tag mimics a cargo protein that cannot be released from PEX5, thus keeping monoubiquitinated PEX5 at the membrane for a sufficiently long time to be recognized by the autophagic machinery. This in turn suggests that monoubiquitination of the N-terminal cysteine of peroxisome-associated PEX5 not only functions to recycle the peroxin back to the cytosol, but also serves as a quality control mechanism to eliminate peroxisomes with a defective protein import machinery.
DOI: 10.6084/m9.figshare.1452908.v1
title: Sexual dimorphism in conspicuousness and ornamentation in an enigmatic lizard from Sri Lanka, the leaf-nosed lizard Ceratophora tennentii

description: This is the entire bitbucket git repository that contains the necessary data, code, figures, tables etc for paper. If just interested in the data itself please just see "Final_Data_Files" within the "Data" folder. The "SpecData.csv" contains the processed spec files for the labial, throat and mouth areas. These were converted from a list to a dataframe in R and so areas need to be subsetted by id. column. All individual ID's are listed as column names and reflectance values are given for wavelengths between 300-700nm. "PerformMorph_data.csv" contains bite force and morphology data for all individuals which we had complete data for. "Morph_data.csv" contains all morphological data on all inidviduals for both sexes.
DOI: 10.6084/m9.figshare.1452914.v3
title: <i>Drosophila</i> Gyf/GRB10 interacting GYF protein is an autophagy regulator that controls neuron and muscle homeostasis

description: Autophagy is an essential process for eliminating ubiquitinated protein aggregates and dysfunctional organelles. Defective autophagy is associated with various degenerative diseases such as Parkinson disease. Through a genetic screening in <i>Drosophila</i>, we identified <i>CG11148</i>, whose product is orthologous to GIGYF1 (GRB10-interacting GYF protein 1) and GIGYF2 in mammals, as a new autophagy regulator; we hereafter refer to this gene as <i>Gyf</i>. Silencing of <i>Gyf</i> completely suppressed the effect of Atg1-Atg13 activation in stimulating autophagic flux and inducing autophagic eye degeneration. Although <i>Gyf</i> silencing did not affect Atg1-induced Atg13 phosphorylation or Atg6-Pi3K59F (class III PtdIns3K)-dependent Fyve puncta formation, it inhibited formation of Atg13 puncta, suggesting that Gyf controls autophagy through regulating subcellular localization of the Atg1-Atg13 complex. <i>Gyf</i> silencing also inhibited Atg1-Atg13-induced formation of Atg9 puncta, which is accumulated upon active membrane trafficking into autophagosomes. <i>Gyf</i>-null mutants also exhibited substantial defects in developmental or starvation-induced accumulation of autophagosomes and autolysosomes in the larval fat body. Furthermore, heads and thoraxes from <i>Gyf</i>-null adults exhibited strongly reduced expression of autophagosome-associated Atg8a-II compared to wild-type (WT) tissues. The decrease in Atg8a-II was directly correlated with an increased accumulation of ubiquitinated proteins and dysfunctional mitochondria in neuron and muscle, which together led to severe locomotor defects and early mortality. These results suggest that Gyf-mediated autophagy regulation is important for maintaining neuromuscular homeostasis and preventing degenerative pathologies of the tissues. Since human mutations in the <i>GIGYF2</i> locus were reported to be associated with a type of familial Parkinson disease, the homeostatic role of Gyf-family proteins is likely to be evolutionarily conserved.
DOI: 10.6084/m9.figshare.1452969.v5
title: (being updated) University of Luxembourg | PhD theses without on-line PhD thesis publications | @ 18/6/2015

description: Via Open Repository and Bibliography Luxembourg (ORBi lu)