cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.4653856.v1
title: Kok2015_Experiment2CELEB_raw from Face familiarity promotes stable identity recognition: exploring face perception using serial dependence

description: Studies suggest that familiar faces are processed in a manner distinct from unfamiliar faces and that familiarity with a face confers an advantage in identity recognition. Our visual system seems to capitalize on experience to build stable face representations that are impervious to variation in retinal input that may occur due to changes in lighting, viewpoint, viewing distance, eye movements, etc. Emerging evidence also suggests that our visual system maintains a continuous perception of a face's identity from one moment to the next despite the retinal input variations through serial dependence. This study investigates whether interactions occur between face familiarity and serial dependence. In two experiments, participants used a continuous scale to rate attractiveness of unfamiliar and familiar faces (either experimentally learned or famous) presented in rapid sequences. Both experiments revealed robust inter-trial effects in which attractiveness ratings for a given face depended on the preceding face's attractiveness. This inter-trial attractiveness effect was most pronounced for unfamiliar faces. Indeed, when participants were familiar with a given face, attractiveness ratings showed significantly less serial dependence. These results represent the first evidence that familiar faces can resist the temporal integration seen in sequential dependencies and highlight the importance of familiarity to visual cognition.
DOI: 10.6084/m9.figshare.4653847
title: Kok2015_Experiment1LEARN_raw from Face familiarity promotes stable identity recognition: exploring face perception using serial dependence

description: Studies suggest that familiar faces are processed in a manner distinct from unfamiliar faces and that familiarity with a face confers an advantage in identity recognition. Our visual system seems to capitalize on experience to build stable face representations that are impervious to variation in retinal input that may occur due to changes in lighting, viewpoint, viewing distance, eye movements, etc. Emerging evidence also suggests that our visual system maintains a continuous perception of a face's identity from one moment to the next despite the retinal input variations through serial dependence. This study investigates whether interactions occur between face familiarity and serial dependence. In two experiments, participants used a continuous scale to rate attractiveness of unfamiliar and familiar faces (either experimentally learned or famous) presented in rapid sequences. Both experiments revealed robust inter-trial effects in which attractiveness ratings for a given face depended on the preceding face's attractiveness. This inter-trial attractiveness effect was most pronounced for unfamiliar faces. Indeed, when participants were familiar with a given face, attractiveness ratings showed significantly less serial dependence. These results represent the first evidence that familiar faces can resist the temporal integration seen in sequential dependencies and highlight the importance of familiarity to visual cognition.
DOI: 10.6084/m9.figshare.4653841
title: Family-transmitted stress in a wild bird

description: Database for 'Family-transmitted stress in a wild bird'
DOI: 10.6084/m9.figshare.4653847.v1
title: Kok2015_Experiment1LEARN_raw from Face familiarity promotes stable identity recognition: exploring face perception using serial dependence

description: Studies suggest that familiar faces are processed in a manner distinct from unfamiliar faces and that familiarity with a face confers an advantage in identity recognition. Our visual system seems to capitalize on experience to build stable face representations that are impervious to variation in retinal input that may occur due to changes in lighting, viewpoint, viewing distance, eye movements, etc. Emerging evidence also suggests that our visual system maintains a continuous perception of a face's identity from one moment to the next despite the retinal input variations through serial dependence. This study investigates whether interactions occur between face familiarity and serial dependence. In two experiments, participants used a continuous scale to rate attractiveness of unfamiliar and familiar faces (either experimentally learned or famous) presented in rapid sequences. Both experiments revealed robust inter-trial effects in which attractiveness ratings for a given face depended on the preceding face's attractiveness. This inter-trial attractiveness effect was most pronounced for unfamiliar faces. Indeed, when participants were familiar with a given face, attractiveness ratings showed significantly less serial dependence. These results represent the first evidence that familiar faces can resist the temporal integration seen in sequential dependencies and highlight the importance of familiarity to visual cognition.
DOI: 10.6084/m9.figshare.4653808
title: Supplementary Material for: Influence of Sunflower Seed Oil on the Skin Barrier Function of Preterm Infants: A Randomized Controlled Trial

description: <b><i>Background:</i></b> Inadequate skin care may increase morbidity in preterm infants. Skin care practices that support skin maturation have barely been investigated. <b><i>Objectives:</i></b> To investigate the effect of sunflower seed oil (SSO) on skin barrier development in low-birth-weight premature infants. <b><i>Methods:</i></b> 22 preterm infants (&lt;48 h after birth, 1,500-2,500 g) were randomized into group C (control) and group SSO, receiving daily SSO application during the first 10 postnatal days, followed by no intervention. Transepidermal water loss (TEWL), stratum corneum hydration (SCH), skin pH and sebum were measured &lt;48 h after birth and on postnatal days 5, 11 and 21 on the forehead, abdomen, thigh and buttock. <b><i>Results:</i></b> Skin pH decreased, while sebum remained stable in both groups. In group C, TEWL remained stable; in group SSO, TEWL increased significantly on the abdomen, leg and buttock until day 11, followed by a decrease after SSO application had been stopped. Abdomen SCH remained stable in group C, but continuously decreased in group SSO until day 21. <b><i>Conclusion:</i></b> SSO application may retard postnatal skin barrier maturation in preterm infants.
DOI: 10.6084/m9.figshare.4653838
title: Supplementary Material for: Clinicopathological Features and Prognostic Significance of HER2 Expression in Gastric Cancer

description: <b><i>Background:</i></b> HER2 positivity is reported to be &lt;20% in gastric cancer. Clinicopathological characteristics will be helpful to understand the biological features of HER2-positive gastric cancer. <b><i>Methods:</i></b> A total of 813 gastric cancer patients who underwent HER2 testing between January 2005 and December 2010 were included in this study. <b><i>Results:</i></b> Ninety-five (11.7%) patients had HER2-positive gastric cancer. Elevated serum carcinoembryonic antigen (CEA) concentration [odds ratio (OR), 5.629; p &lt; 0.001] and differentiated histology (OR, 3.717; p = 0.002) were significant predictive factors for HER2 positivity in localized disease. For recurrent or metastatic disease, elevated serum CEA concentration (OR, 2.545; p &lt; 0.001), differentiated histology (OR, 3.299; p &lt; 0.001), pulmonary metastasis (OR, 3.321; p = 0.001), and distant lymph node metastasis (OR, 2.286; p = 0.002) were significant predictive factors. Median disease-free survival (DFS) was shorter in HER2-positive patients than in others, especially in stage I or II disease (24.7 vs. 49.2 months; p &lt; 0.001). Among HER2-negative patients with stage II diseases, patients who received adjuvant chemotherapy had longer DFS than others (42.2 vs. 30.7 months; p = 0.025). <b><i>Conclusions:</i></b> Clinicopathological factors may be useful in predicting the HER2 positivity of gastric cancer. Further studies are needed to understand the molecular basis of HER2-positive gastric cancer.
DOI: 10.17632/f666xk8frd.1
title: Classification of Two Distinct Wound Types in Recessive Dystrophic Epidermolysis Bullosa: A Retrospective Natural History Study

description: Supplemental material
DOI: 10.6084/m9.figshare.4653709
title: Supplementary Material for: Helicobacter pylori Inhibits Dendritic Cell Maturation via Interleukin-10-Mediated Activation of the Signal Transducer and Activator of Transcription 3 Pathway

description: <i>Helicobacter pylori</i> infects the human gastric mucosa causing a chronic infection that is the primary risk factor for gastric cancer development. Recent studies demonstrate that <i>H. pylori</i> promotes tolerogenic dendritic cell (DC) development indicating that this bacterium evades the host immune response. However, the signaling pathways involved in modulating DC activation during infection remain unclear. Here, we report that<i> H. pylori</i> infection activated the signal transducer and activator of transcription 3 (STAT3) pathway in murine bone marrow-derived DCs (BMDCs) and splenic DCs isolated ex vivo. Isogenic <i>cagA-</i>, <i>cagE-</i>, <i>vacA-</i> and urease-mutants exhibited levels of phosphoSTAT3 that were comparable to in the wild-type (WT) parent strain. <i>H. pylori</i>-infected BMDCs produced increased immunosuppressive IL-10, which activated STAT3 in an autocrine/paracrine fashion. Neutralization of IL-10 prevented <i>H. pylori</i>-mediated STAT3 activation in both BMDCs and splenic DCs. In addition, anti-IL-10 treatment of infected <i>H. pylori</i>-BMDCs was associated with increased CD86 and MHC II expression and enhanced proinflammatory IL-1β cytokine secretion. Finally, increased CD86 and MHC II expression was detected in <i>H. pylori</i>-infected STAT3 knockout DCs when compared to WT controls. Together, these results demonstrate that <i>H. pylori</i> infection induces IL-10 secretion in DCs, which activates STAT3, thereby modulating DC maturation and reducing IL-1β secretion. These findings identify a host molecular mechanism by which <i>H. pylori</i> can manipulate the innate immune response to potentially favor chronic infection and promote carcinogenesis.
DOI: 10.6084/m9.figshare.4653733
title: Supplementary Material for: The Janus Face of a-Toxin: A Potent Mediator of Cytoprotection in Staphylococci-Infected Macrophages

description: After phagocytosis by macrophages, <i>Staphylococcus aureus</i> evades killing in an a-toxin-dependent manner, and then prevents apoptosis of infected cells by upregulating expression of antiapoptotic genes like <i>MCL-1 (myeloid cell leukemia-1)</i>. Here, using purified a-toxin and a set of <i>hla</i>-deficient strains, we show that a-toxin is critical for the induction of <i>MCL-1 </i>expression and the cytoprotection of infected macrophages. Extracellular or intracellular treatment of macrophages with a-toxin alone did not induce cytoprotection conferred by increased Mcl-1, suggesting that the process is dependent on the production of a-toxin by intracellular bacteria. The increased expression of <i>MCL-1</i> in infected cells was associated with enhanced NFκB activation, and subsequent IL-6 secretion. This effect was only partially inhibited by blocking TLR2, which suggests the participation of intracellular receptors in the specific recognition of <i>S. aureus </i>strains secreting a-toxin. Thus, <i>S. aureus</i> recognition by intracellular receptors and/or activation of downstream pathways leading to Mcl-1 expression is facilitated by a-toxin released by intracellular bacteria which permeabilize phagosomes, ensuring pathogen access to the cytoplasmatic compartment. Given that the intracellular survival of <i>S. aureus</i> depends on a-toxin, we propose a novel role for this agent in the protection of the intracellular niche, and further dissemination of staphylococci by infected macrophages.
DOI: 10.6084/m9.figshare.4653709.v1
title: Supplementary Material for: Helicobacter pylori Inhibits Dendritic Cell Maturation via Interleukin-10-Mediated Activation of the Signal Transducer and Activator of Transcription 3 Pathway

description: <i>Helicobacter pylori</i> infects the human gastric mucosa causing a chronic infection that is the primary risk factor for gastric cancer development. Recent studies demonstrate that <i>H. pylori</i> promotes tolerogenic dendritic cell (DC) development indicating that this bacterium evades the host immune response. However, the signaling pathways involved in modulating DC activation during infection remain unclear. Here, we report that<i> H. pylori</i> infection activated the signal transducer and activator of transcription 3 (STAT3) pathway in murine bone marrow-derived DCs (BMDCs) and splenic DCs isolated ex vivo. Isogenic <i>cagA-</i>, <i>cagE-</i>, <i>vacA-</i> and urease-mutants exhibited levels of phosphoSTAT3 that were comparable to in the wild-type (WT) parent strain. <i>H. pylori</i>-infected BMDCs produced increased immunosuppressive IL-10, which activated STAT3 in an autocrine/paracrine fashion. Neutralization of IL-10 prevented <i>H. pylori</i>-mediated STAT3 activation in both BMDCs and splenic DCs. In addition, anti-IL-10 treatment of infected <i>H. pylori</i>-BMDCs was associated with increased CD86 and MHC II expression and enhanced proinflammatory IL-1β cytokine secretion. Finally, increased CD86 and MHC II expression was detected in <i>H. pylori</i>-infected STAT3 knockout DCs when compared to WT controls. Together, these results demonstrate that <i>H. pylori</i> infection induces IL-10 secretion in DCs, which activates STAT3, thereby modulating DC maturation and reducing IL-1β secretion. These findings identify a host molecular mechanism by which <i>H. pylori</i> can manipulate the innate immune response to potentially favor chronic infection and promote carcinogenesis.
DOI: 10.6084/m9.figshare.4653685
title: PowerPoint Slides for: Renal Function and Scaled Troponin in Patients Presenting to the Emergency Department with Symptoms of Myocardial Infarction

description: <b><i>Background:</i></b> Cardiac troponins are often found to be elevated in patients with renal dysfunction, even in the absence of acute myocardial injury. The objective of this report was to characterize the scaled troponin values and proportion of adjudicated acute myocardial infarction (AMI) among patients with and without renal dysfunction. <b><i>Methods:</i></b> The data was from a multicenter prospective study including patients presenting to the emergency department with symptoms of AMI. Troponin measurements were standardized across various assays by calculating the observed results as multiples of the assay-specific 99th percentile upper limit of normal. Patients with an estimated glomerular filtration rate (eGFR; calculated by the Chronic Kidney Disease Epidemiology Collaboration formula) &lt;60 mL/min/1.73 m<sup>2</sup> were considered to have renal dysfunction. <b><i>Results:</i></b> Of 430 included patients, 249 (58%) were male and 181 (42%) were female, with a mean age of 55.9 ± 12.3 and 57.3 ± 12.8 years, respectively. Eighty-seven (20.2%) had renal dysfunction. The proportions of patients with at least one scaled troponin value above the 99th percentile cut-off point among patients with and without renal dysfunction were 40 (45.9%) and 81 (23.6%) respectively (<i>p</i> &lt; 0.001). The proportions of patients with an adjudicated diagnosis of AMI among those with and without renal dysfunction were 20.7 and 18.7%, respectively (<i>p</i> = 0.67). Using scaled troponins, by the second test there was &gt;5X and by the third test &gt;15X separation in the excursion of troponin among those with AMI compared to those without. <b><i>Conclusions:</i></b> One or more elevated troponin values are common in those with renal dysfunction. Scaled troponins for eGFR groups were similar, indicating that the use of this interpretative technique is applicable in discerning AMI for those with and without renal dysfunction.
DOI: 10.6084/m9.figshare.4653685.v1
title: PowerPoint Slides for: Renal Function and Scaled Troponin in Patients Presenting to the Emergency Department with Symptoms of Myocardial Infarction

description: <b><i>Background:</i></b> Cardiac troponins are often found to be elevated in patients with renal dysfunction, even in the absence of acute myocardial injury. The objective of this report was to characterize the scaled troponin values and proportion of adjudicated acute myocardial infarction (AMI) among patients with and without renal dysfunction. <b><i>Methods:</i></b> The data was from a multicenter prospective study including patients presenting to the emergency department with symptoms of AMI. Troponin measurements were standardized across various assays by calculating the observed results as multiples of the assay-specific 99th percentile upper limit of normal. Patients with an estimated glomerular filtration rate (eGFR; calculated by the Chronic Kidney Disease Epidemiology Collaboration formula) &lt;60 mL/min/1.73 m<sup>2</sup> were considered to have renal dysfunction. <b><i>Results:</i></b> Of 430 included patients, 249 (58%) were male and 181 (42%) were female, with a mean age of 55.9 ± 12.3 and 57.3 ± 12.8 years, respectively. Eighty-seven (20.2%) had renal dysfunction. The proportions of patients with at least one scaled troponin value above the 99th percentile cut-off point among patients with and without renal dysfunction were 40 (45.9%) and 81 (23.6%) respectively (<i>p</i> &lt; 0.001). The proportions of patients with an adjudicated diagnosis of AMI among those with and without renal dysfunction were 20.7 and 18.7%, respectively (<i>p</i> = 0.67). Using scaled troponins, by the second test there was &gt;5X and by the third test &gt;15X separation in the excursion of troponin among those with AMI compared to those without. <b><i>Conclusions:</i></b> One or more elevated troponin values are common in those with renal dysfunction. Scaled troponins for eGFR groups were similar, indicating that the use of this interpretative technique is applicable in discerning AMI for those with and without renal dysfunction.
DOI: 10.6084/m9.figshare.4653622
title: Phylogenetic workflow for detection of HGT

description: Perl script for detection of HGT
DOI: 10.6084/m9.figshare.4653586
title: Micromeasure Data 2017

description: Raw data obtained with Micromeasure on 1001 spermatocytes from 7 boars, studied by immunocytological approaches (MLH1, SCP1, SCP3).
DOI: 10.6084/m9.figshare.4653604
title: cafe zazou

description: café sur les données de diversité de zazou :)<br>
DOI: 10.6084/m9.figshare.4653604.v1
title: cafe zazou

description: café sur les données de diversité de zazou :)<br>
DOI: 10.6084/m9.figshare.4653586.v2
title: Micromeasure Data 2017

description: Raw data obtained with Micromeasure on 1001 spermatocytes from 7 boars, studied by immunocytological approaches (MLH1, SCP1, SCP3).
DOI: 10.6084/m9.figshare.4653541
title: Table S2 from Parallel analysis of Arabidopsis circadian clock mutants reveals different scales of transcriptome and proteome regulation

description: The circadian clock regulates physiological processes central to growth and survival. To date, most plant circadian clock studies have relied on diurnal transcriptome changes to elucidate molecular connections between the circadian clock and observable phenotypes in wild-type plants. Here, we have integrated RNA-sequencing and protein mass spectrometry data to comparatively analyse the <i>lhycca1</i>, <i>prr7prr9</i>, <i>gi</i> and <i>toc1</i> circadian clock mutant rosette at the end of day and end of night. Each mutant affects specific sets of genes and proteins, suggesting that the circadian clock regulation is modular. Furthermore, each circadian clock mutant maintains its own dynamically fluctuating transcriptome and proteome profile specific to subcellular compartments. Most of the measured protein levels do not correlate with changes in their corresponding transcripts. Transcripts and proteins that have coordinated changes in abundance are enriched for carbohydrate- and cold-responsive genes. Transcriptome changes in all four circadian clock mutants also affect genes encoding starch degradation enzymes, transcription factors and protein kinases. The comprehensive transcriptome and proteome datasets demonstrate that future system-driven research of the circadian clock requires multi-level experimental approaches. Our work also shows that further work is needed to elucidate the roles of post-translational modifications and protein degradation in the regulation of clock-related processes.
DOI: 10.6084/m9.figshare.4653586.v1
title: Data_mary2017

description: Raw data obtained with Micromeasure on 1001 spermatocytes from 7 boars, studied by immunocytological approaches (MLH1, SCP1, SCP3).
DOI: 10.6084/m9.figshare.4653535
title: Table S3 from Parallel analysis of Arabidopsis circadian clock mutants reveals different scales of transcriptome and proteome regulation

description: The circadian clock regulates physiological processes central to growth and survival. To date, most plant circadian clock studies have relied on diurnal transcriptome changes to elucidate molecular connections between the circadian clock and observable phenotypes in wild-type plants. Here, we have integrated RNA-sequencing and protein mass spectrometry data to comparatively analyse the <i>lhycca1</i>, <i>prr7prr9</i>, <i>gi</i> and <i>toc1</i> circadian clock mutant rosette at the end of day and end of night. Each mutant affects specific sets of genes and proteins, suggesting that the circadian clock regulation is modular. Furthermore, each circadian clock mutant maintains its own dynamically fluctuating transcriptome and proteome profile specific to subcellular compartments. Most of the measured protein levels do not correlate with changes in their corresponding transcripts. Transcripts and proteins that have coordinated changes in abundance are enriched for carbohydrate- and cold-responsive genes. Transcriptome changes in all four circadian clock mutants also affect genes encoding starch degradation enzymes, transcription factors and protein kinases. The comprehensive transcriptome and proteome datasets demonstrate that future system-driven research of the circadian clock requires multi-level experimental approaches. Our work also shows that further work is needed to elucidate the roles of post-translational modifications and protein degradation in the regulation of clock-related processes.
DOI: 10.6084/m9.figshare.4653541.v1
title: Table S2 from Parallel analysis of Arabidopsis circadian clock mutants reveals different scales of transcriptome and proteome regulation

description: The circadian clock regulates physiological processes central to growth and survival. To date, most plant circadian clock studies have relied on diurnal transcriptome changes to elucidate molecular connections between the circadian clock and observable phenotypes in wild-type plants. Here, we have integrated RNA-sequencing and protein mass spectrometry data to comparatively analyse the <i>lhycca1</i>, <i>prr7prr9</i>, <i>gi</i> and <i>toc1</i> circadian clock mutant rosette at the end of day and end of night. Each mutant affects specific sets of genes and proteins, suggesting that the circadian clock regulation is modular. Furthermore, each circadian clock mutant maintains its own dynamically fluctuating transcriptome and proteome profile specific to subcellular compartments. Most of the measured protein levels do not correlate with changes in their corresponding transcripts. Transcripts and proteins that have coordinated changes in abundance are enriched for carbohydrate- and cold-responsive genes. Transcriptome changes in all four circadian clock mutants also affect genes encoding starch degradation enzymes, transcription factors and protein kinases. The comprehensive transcriptome and proteome datasets demonstrate that future system-driven research of the circadian clock requires multi-level experimental approaches. Our work also shows that further work is needed to elucidate the roles of post-translational modifications and protein degradation in the regulation of clock-related processes.