cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1568234
title: Does a global DNA barcoding gap exist in Annelida?

description: Accurate identification of unknown specimens by means of DNA barcoding is contingent on the presence of a DNA barcoding gap, among other factors, as its absence may result in dubious specimen identifications – false negatives or positives. Whereas the utility of DNA barcoding would be greatly reduced in the absence of a distinct and sufficiently sized barcoding gap, the limits of intraspecific and interspecific distances are seldom thoroughly inspected across comprehensive sampling. The present study aims to illuminate this aspect of barcoding in a comprehensive manner for the animal phylum Annelida. All cytochrome <i>c</i> oxidase subunit I sequences (<i>cox1</i> gene; the chosen region for zoological DNA barcoding) present in GenBank for Annelida, as well as for “Polychaeta”, “Oligochaeta”, and Hirudinea separately, were downloaded and curated for length, coverage and potential contaminations. The final datasets consisted of 9782 (Annelida), 5545 (“Polychaeta”), 3639 (“Oligochaeta”), and 598 (Hirudinea) <i>cox1</i> sequences and these were either (i) used as is in an automated global barcoding gap detection analysis or (ii) further analyzed for genetic distances, separated into bins containing intraspecific and interspecific comparisons and plotted in a graph to visualize any potential global barcoding gap. Over 70 million pairwise genetic comparisons were made and results suggest that although there is a tendency towards separation, no distinct or sufficiently sized global barcoding gap exists in either of the datasets rendering future barcoding efforts at risk of erroneous specimen identifications (but local barcoding gaps may still exist allowing for the identification of specimens at lower taxonomic ranks). This seems to be especially true for earthworm taxa, which account for fully 35% of the total number of interspecific comparisons that show 0% divergence.
DOI: 10.6084/m9.figshare.1568234.v1
title: Does a global DNA barcoding gap exist in Annelida?

description: Accurate identification of unknown specimens by means of DNA barcoding is contingent on the presence of a DNA barcoding gap, among other factors, as its absence may result in dubious specimen identifications – false negatives or positives. Whereas the utility of DNA barcoding would be greatly reduced in the absence of a distinct and sufficiently sized barcoding gap, the limits of intraspecific and interspecific distances are seldom thoroughly inspected across comprehensive sampling. The present study aims to illuminate this aspect of barcoding in a comprehensive manner for the animal phylum Annelida. All cytochrome <i>c</i> oxidase subunit I sequences (<i>cox1</i> gene; the chosen region for zoological DNA barcoding) present in GenBank for Annelida, as well as for “Polychaeta”, “Oligochaeta”, and Hirudinea separately, were downloaded and curated for length, coverage and potential contaminations. The final datasets consisted of 9782 (Annelida), 5545 (“Polychaeta”), 3639 (“Oligochaeta”), and 598 (Hirudinea) <i>cox1</i> sequences and these were either (i) used as is in an automated global barcoding gap detection analysis or (ii) further analyzed for genetic distances, separated into bins containing intraspecific and interspecific comparisons and plotted in a graph to visualize any potential global barcoding gap. Over 70 million pairwise genetic comparisons were made and results suggest that although there is a tendency towards separation, no distinct or sufficiently sized global barcoding gap exists in either of the datasets rendering future barcoding efforts at risk of erroneous specimen identifications (but local barcoding gaps may still exist allowing for the identification of specimens at lower taxonomic ranks). This seems to be especially true for earthworm taxa, which account for fully 35% of the total number of interspecific comparisons that show 0% divergence.
DOI: 10.6084/m9.figshare.1568238.v1
title: Performance evaluation of head and neck contour adaptation with cone beam CT using two commercial software systems

description: Performance evaluation of head and neck contour adaptation with cone beam CT using two commercial software systems
DOI: 10.6084/m9.figshare.1568238.v3
title: Performance evaluation of head and neck contour adaptation with cone beam CT using two commercial software systems

description: Performance evaluation of head and neck contour adaptation with cone beam CT using two commercial software systems
DOI: 10.6084/m9.figshare.1568238.v2
title: Performance evaluation of head and neck contour adaptation with cone beam CT using two commercial software systems

description: Performance evaluation of head and neck contour adaptation with cone beam CT using two commercial software systems
DOI: 10.6084/m9.figshare.1568226
title: Transport of gaseous pollutants by convective boundary layer around a human body

description: This study investigates the ability of the human convective boundary layer to transport pollution in a quiescent indoor environment. The impact of the source location in the vicinity of a human body is examined in relation to pollution distribution in the breathing zone and the thickness of the pollution boundary layer. The study, in addition, evaluates the effects of the room air temperature, table positioning, and seated body inclination. The human body is represented by a thermal manikin that has a body shape, size, and surface temperature that resemble those of a real person. The results show that the source location has a considerable influence on the breathing zone pollution concentrations and on the thickness of the pollution boundary layer. The highest breathing zone concentrations are achieved when the pollution is located at the chest, while there is negligible exposure for the pollution emitted at the upper back or behind the chair. The results also indicate that a decrease in personal exposure to pollutants released from or around the human body increases the extent to which the pollution spreads to the surroundings. Reducing the room air temperature or backward body inclination intensifies the transport of the pollution to the breathing zone and increases personal exposure. The front edge of a table positioned at zero distance from the human body can reduce the pollution transport to the breathing zone, or it can increase transport of the clean air from beneath if positioned at a 10-cm (0.33-ft) distance.
DOI: 10.6084/m9.figshare.1568226.v2
title: Transport of gaseous pollutants by convective boundary layer around a human body

description: This study investigates the ability of the human convective boundary layer to transport pollution in a quiescent indoor environment. The impact of the source location in the vicinity of a human body is examined in relation to pollution distribution in the breathing zone and the thickness of the pollution boundary layer. The study, in addition, evaluates the effects of the room air temperature, table positioning, and seated body inclination. The human body is represented by a thermal manikin that has a body shape, size, and surface temperature that resemble those of a real person. The results show that the source location has a considerable influence on the breathing zone pollution concentrations and on the thickness of the pollution boundary layer. The highest breathing zone concentrations are achieved when the pollution is located at the chest, while there is negligible exposure for the pollution emitted at the upper back or behind the chair. The results also indicate that a decrease in personal exposure to pollutants released from or around the human body increases the extent to which the pollution spreads to the surroundings. Reducing the room air temperature or backward body inclination intensifies the transport of the pollution to the breathing zone and increases personal exposure. The front edge of a table positioned at zero distance from the human body can reduce the pollution transport to the breathing zone, or it can increase transport of the clean air from beneath if positioned at a 10-cm (0.33-ft) distance.
DOI: 10.6084/m9.figshare.1568226.v1
title: Transport of gaseous pollutants by convective boundary layer around a human body

description: This study investigates the ability of the human convective boundary layer to transport pollution in a quiescent indoor environment. The impact of the source location in the vicinity of a human body is examined in relation to pollution distribution in the breathing zone and the thickness of the pollution boundary layer. The study, in addition, evaluates the effects of the room air temperature, table positioning, and seated body inclination. The human body is represented by a thermal manikin that has a body shape, size, and surface temperature that resemble those of a real person. The results show that the source location has a considerable influence on the breathing zone pollution concentrations and on the thickness of the pollution boundary layer. The highest breathing zone concentrations are achieved when the pollution is located at the chest, while there is negligible exposure for the pollution emitted at the upper back or behind the chair. The results also indicate that a decrease in personal exposure to pollutants released from or around the human body increases the extent to which the pollution spreads to the surroundings. Reducing the room air temperature or backward body inclination intensifies the transport of the pollution to the breathing zone and increases personal exposure. The front edge of a table positioned at zero distance from the human body can reduce the pollution transport to the breathing zone, or it can increase transport of the clean air from beneath if positioned at a 10-cm (0.33-ft) distance.
DOI: 10.6084/m9.figshare.1568222
title: Effect of <i>Prosopis</i> (mesquite) invasion and clearing on vegetation cover in semi-arid Nama Karoo rangeland, South Africa

description: The Nama-Karoo is the largest of the three biomes that comprise the semi-arid Karoo-Namib ecoregion of southern Africa. Large tracts of Nama-Karoo rangeland have been invaded by alien leguminous trees of the genus <i>Prosopis</i>. We assessed the impact of <i>Prosopis</i> invasion and clearing on vegetation cover in heavily grazed Nama-Karoo rangeland on two sheep farms in the Beaufort West district of the Western Cape province of South Africa. Our results suggest that, below critical threshold cover levels, <i>Prosopis</i> trees do not affect indigenous vegetation and add to overall rangeland vegetation cover. However, once <i>Prosopis</i> cover exceeds critical thresholds, the trees begin to negatively impact on indigenous vegetation (especially grasses) and overall vegetation cover. In addition, our data suggest that vegetation cover recovers after <i>Prosopis</i> clearing, being temporarily higher than pre-invasion levels possibly as a result of enhanced post-invasion soil fertility. Lastly, our results suggest that <i>Prosopis</i> trees reduce rangeland erosion potential at low cover and increase it after they exceed critical threshold cover. Information about thresholds of <i>Prosopis</i> impact can be used to direct clearing efforts for maximum benefit when resources are limited.
DOI: 10.6084/m9.figshare.1568222.v2
title: Effect of <i>Prosopis</i> (mesquite) invasion and clearing on vegetation cover in semi-arid Nama Karoo rangeland, South Africa

description: The Nama-Karoo is the largest of the three biomes that comprise the semi-arid Karoo-Namib ecoregion of southern Africa. Large tracts of Nama-Karoo rangeland have been invaded by alien leguminous trees of the genus <i>Prosopis</i>. We assessed the impact of <i>Prosopis</i> invasion and clearing on vegetation cover in heavily grazed Nama-Karoo rangeland on two sheep farms in the Beaufort West district of the Western Cape province of South Africa. Our results suggest that, below critical threshold cover levels, <i>Prosopis</i> trees do not affect indigenous vegetation and add to overall rangeland vegetation cover. However, once <i>Prosopis</i> cover exceeds critical thresholds, the trees begin to negatively impact on indigenous vegetation (especially grasses) and overall vegetation cover. In addition, our data suggest that vegetation cover recovers after <i>Prosopis</i> clearing, being temporarily higher than pre-invasion levels possibly as a result of enhanced post-invasion soil fertility. Lastly, our results suggest that <i>Prosopis</i> trees reduce rangeland erosion potential at low cover and increase it after they exceed critical threshold cover. Information about thresholds of <i>Prosopis</i> impact can be used to direct clearing efforts for maximum benefit when resources are limited.
DOI: 10.6084/m9.figshare.1568218.v1
title: Activation of autophagy in macrophages by pro-resolving lipid mediators

description: The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA<sub>4</sub> and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA<sub>4</sub> and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3<sup>+</sup> autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA<sub>4</sub> and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages <i>via</i> NFE2L2. Therefore, 15-epi-LXA<sub>4</sub> and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.
DOI: 10.6084/m9.figshare.1568218.v2
title: Activation of autophagy in macrophages by pro-resolving lipid mediators

description: The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA<sub>4</sub> and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA<sub>4</sub> and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3<sup>+</sup> autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA<sub>4</sub> and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA<sub>4</sub> and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.
DOI: 10.6084/m9.figshare.1568218.v3
title: Activation of autophagy in macrophages by pro-resolving lipid mediators

description: The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA<sub>4</sub> and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA<sub>4</sub> and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3<sup>+</sup> autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA<sub>4</sub> and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA<sub>4</sub> and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.
DOI: 10.6084/m9.figshare.1568218
title: Activation of autophagy in macrophages by pro-resolving lipid mediators

description: The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA<sub>4</sub> and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA<sub>4</sub> and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3<sup>+</sup> autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA<sub>4</sub> and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA<sub>4</sub> and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.
DOI: 10.6084/m9.figshare.1568218.v5
title: Activation of autophagy in macrophages by pro-resolving lipid mediators

description: The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA<sub>4</sub> and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA<sub>4</sub> and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3<sup>+</sup> autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA<sub>4</sub> and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA<sub>4</sub> and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.
DOI: 10.6084/m9.figshare.1568207
title: Diurnal emotional reactivity: Ultradian changes at neural and behavioral levels in men

description: The aim of this study was to examine the ultradian dynamic of emotional processing in men. Event-related potentials were recorded while participants watched different sets of unpleasant and neutral pictures every 15 min for 3 h. Emotional feelings induced by unpleasant pictures were also assessed with self-rating scales at the end of each picture set. Whereas brain processing of neutral pictures remained stable over time, a late positive component elicited by unpleasant pictures presented ultradian oscillations varying between 65 and 110 min in 77% of the participants, mainly in the right centro-posterior area. Ultradian rhythms were also observed for values self-rating the intensity of unpleasant feelings. Correlative analyses performed between brain and behavioral ultradian oscillations indicated that these rhythms follow a temporal opposite pattern. For the first time, these results raise questions regarding the modulating role of ultradian oscillations when the brain computes the significance of unpleasant stimuli and produces the final emotional feelings. Overall, these findings open new perspectives on the temporal regulation of emotional reactivity in healthy individuals and in those with affective disorders.
DOI: 10.6084/m9.figshare.1568218.v4
title: Activation of autophagy in macrophages by pro-resolving lipid mediators

description: The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA<sub>4</sub> and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA<sub>4</sub> and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3<sup>+</sup> autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA<sub>4</sub> and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA<sub>4</sub> and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.