cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3187627
title: Scholarship, Collaboration, and Data

description: Science and Scholarship is changing. To change with it, we need to study it. To study it we need open data regarding scholarship. In particular, we need global persistent identifiers, common data models and terminology, and a shared community vision of open data regarding scholarship.
DOI: 10.6084/m9.figshare.3187685.v4
title: 2014 07 22 VID00001 Enhanced Frames No Denoise

description: Segment of frames of VID00001 taken on 22 July 2014. Frames bracket the best single frame at VID00001 0 20 28-60. Frames are extracted using Cisco FlipShare software distributed with the Cisco Flip UltraHD 720p digital video recorder used to record the video. Frames are then enhanced using Adobe Photoshop Creative Cloud as follows:1) Image Size; Width 300%; Resolution: 300 per inch; With Scale Styles; With Constrain Proportions; Interpolation: preserve details; Noise: 0.2) Save; As: PNG Format; Interlace: None; Filter: Adaptive; Compression: 9.These settings best preserve fine details through the enlargement process.<br><br>Project order 34a<b></b><i></i><sub></sub><sup></sup><br><br>
DOI: 10.6084/m9.figshare.3187655.v2
title: 2014 09 20 VID00043 Enhanced Frames No Denoise

description: Every frame of VID00043 taken on 20 September 2014. Frames are extracted using Cisco FlipShare software distributed with the Cisco Flip UltraHD 720p digital video recorder used to record the video. Frames are then enhanced using Adobe Photoshop Creative Cloud as follows:1) Image Size; Width 300%; Resolution: 300 per inch; With Scale Styles; With Constrain Proportions; Interpolation: preserve details; Noise: 0.2) Save; As: PNG Format; Interlace: None; Filter: Adaptive; Compression: 9.These settings best preserve fine details through the enlargement process.<br><br>Project order 46a<br>
DOI: 10.6084/m9.figshare.3187655.v1
title: 20 September 2014 VID00043 Enhanced Frames No Denoise

description: Every frame of VID00043 taken on 20 September 2014. Frames are extracted using Cisco FlipShare software distributed with the Cisco Flip UltraHD 720p digital video recorder used to record the video. Frames are then enhanced using Adobe Photoshop Creative Cloud as follows:1) Image Size; Width 300%; Resolution: 300 per inch; With Scale Styles; With Constrain Proportions; Interpolation: preserve details; Noise: 0.2) Save; As: PNG Format; Interlace: None; Filter: Adaptive; Compression: 9.These settings best preserve fine details through the enlargement process.<br>
DOI: 10.6084/m9.figshare.3187685.v3
title: 2014 07 July 2014 VID00001 Enhanced Frames No Denoise

description: Segment of frames of VID00001 taken on 22 July 2014. Frames bracket the best single frame at VID00001 0 20 28-60. Frames are extracted using Cisco FlipShare software distributed with the Cisco Flip UltraHD 720p digital video recorder used to record the video. Frames are then enhanced using Adobe Photoshop Creative Cloud as follows:1) Image Size; Width 300%; Resolution: 300 per inch; With Scale Styles; With Constrain Proportions; Interpolation: preserve details; Noise: 0.2) Save; As: PNG Format; Interlace: None; Filter: Adaptive; Compression: 9.These settings best preserve fine details through the enlargement process.<br><br>Project order 34a<b></b><i></i><sub></sub><sup></sup><br><br>
DOI: 10.6084/m9.figshare.3187627.v2
title: Scholarship, Collaboration, and Data

description: Science and Scholarship is changing. To change with it, we need to study it. To study it we need open data regarding scholarship. In particular, we need global persistent identifiers, common data models and terminology, and a shared community vision of open data regarding scholarship.
DOI: 10.6084/m9.figshare.3187611
title: The biofilm matrix of <i>Campylobacter jejuni</i> determined by fluorescence lectin-binding analysis

description: <i>Campylobacter jejuni</i> is responsible for the most common bacterial foodborne gastroenteritis. Despite its fastidious growth, it can survive harsh conditions through biofilm formation. In this work, fluorescence lectin-binding analysis was used to determine the glycoconjugates present in the biofilm matrix of two well-described strains. Screening of 72 lectins revealed strain-specific patterns with six lectins interacting with the biofilm matrix of both strains. The most common sugar moiety contained galactose and <i>N</i>-acetylgalactosamine. Several lectins interacted with <i>N</i>-acetylglucosamine and sialic acid, probably originated from the capsular polysaccharides, lipooligosaccharides and <i>N</i>-glycans of <i>C. jejuni</i>. In addition, glycoconjugates containing mannose and fucose were detected within the biofilm, which have not previously been found in the <i>C. jejuni</i> envelope. Detection of thioflavin T and curcumin highlighted the presence of amyloids in the cell envelope without association with specific cell appendages. The lectins ECA, GS-I, HMA and LEA constitute a reliable cocktail to detect the biofilm matrix of <i>C. jejuni.</i>
DOI: 10.6084/m9.figshare.3187611.v1
title: The biofilm matrix of <i>Campylobacter jejuni</i> determined by fluorescence lectin-binding analysis

description: <i>Campylobacter jejuni</i> is responsible for the most common bacterial foodborne gastroenteritis. Despite its fastidious growth, it can survive harsh conditions through biofilm formation. In this work, fluorescence lectin-binding analysis was used to determine the glycoconjugates present in the biofilm matrix of two well-described strains. Screening of 72 lectins revealed strain-specific patterns with six lectins interacting with the biofilm matrix of both strains. The most common sugar moiety contained galactose and <i>N</i>-acetylgalactosamine. Several lectins interacted with <i>N</i>-acetylglucosamine and sialic acid, probably originated from the capsular polysaccharides, lipooligosaccharides and <i>N</i>-glycans of <i>C. jejuni</i>. In addition, glycoconjugates containing mannose and fucose were detected within the biofilm, which have not previously been found in the <i>C. jejuni</i> envelope. Detection of thioflavin T and curcumin highlighted the presence of amyloids in the cell envelope without association with specific cell appendages. The lectins ECA, GS-I, HMA and LEA constitute a reliable cocktail to detect the biofilm matrix of <i>C. jejuni.</i>
DOI: 10.6084/m9.figshare.3187627.v1
title: Scholarship, Collaboration, and Data

description: Science and Scholarship is changing. To change with it, we need to study it. To study it we need open data regarding scholarship. In particular, we need global persistent identifiers, common data models and terminology, and a shared community vision of open data regarding scholarship.
DOI: 10.6084/m9.figshare.3187603
title: SciENcv-OpenRIF Integration

description: This presentation was given as part of the OpenRIF workshop on April 17, 2016 at the FORCE2016 conference. It provides background on the SciENcv system, the goals of integrating it with OpenRIF, and some details on how the integration is being accomplished.<br>
DOI: 10.6084/m9.figshare.3187591
title: Asthma in Asia: Physician perspectives on control, inhaler use and patient communications

description: <i>Objective:</i> We examined the physician perspectives on asthma management in Asia. <i>Methods:</i> An online/face-to-face, questionnaire-based survey of respiratory specialists and primary care physicians from eight Asian countries/region was carried out. The survey explored asthma control, inhaler selection, technique and use; physician-patient communications and asthma education. Inclusion criteria were &gt;50% of practice time spent on direct patient care; and treated &gt;30 patients with asthma per month, of which &gt;60% were aged &gt;12 years. <i>Results:</i> REALISE Asia (Phase 2) involved 375 physicians with average 15.9(±6.8) years of clinical experience. 89.1% of physicians reporting use of guidelines estimated that 53.2% of their patients have well-controlled (GINA-defined) asthma. Top consideration for inhaler choice was asthma severity (82.4%) and lowest, socio-economic status (32.5%). Then 54.7% of physicians checked their patients’ inhaler techniques during consultations but 28.2(±19.1)% of patients were using their inhalers incorrectly; 21.1–57.9% of physicians could spot improper inhaler techniques in video demonstrations. And 79.6% of physicians believed combination inhalers could increase adherence because of convenience (53.7%), efficacy (52.7%) and usability (18.9%). Initial and follow-up consultations took 16.8(±8.4) and 9.2(±5.3) minutes, respectively. Most (85.1%) physicians used verbal conversations and least (24.5%), video demonstrations of inhaler use; 56.8% agreed that patient attitudes influenced their treatment approach. <i>Conclusion:</i> Physicians and patients have different views of ‘well-controlled’ asthma. Although physicians informed patients about asthma and inhaler usage, they overestimated actual usage and patients’ knowledge was sub-optimal. Physician-patient interactions can be augmented with understanding of patient attitudes, visual aids and ancillary support to perform physical demonstrations to improve treatment outcomes.
DOI: 10.6084/m9.figshare.3187591.v2
title: Asthma in Asia: Physician perspectives on control, inhaler use and patient communications

description: <i>Objective:</i> We examined the physician perspectives on asthma management in Asia. <i>Methods:</i> An online/face-to-face, questionnaire-based survey of respiratory specialists and primary care physicians from eight Asian countries/region was carried out. The survey explored asthma control, inhaler selection, technique and use; physician-patient communications and asthma education. Inclusion criteria were &gt;50% of practice time spent on direct patient care; and treated &gt;30 patients with asthma per month, of which &gt;60% were aged &gt;12 years. <i>Results:</i> REALISE Asia (Phase 2) involved 375 physicians with average 15.9(±6.8) years of clinical experience. 89.1% of physicians reporting use of guidelines estimated that 53.2% of their patients have well-controlled (GINA-defined) asthma. Top consideration for inhaler choice was asthma severity (82.4%) and lowest, socio-economic status (32.5%). Then 54.7% of physicians checked their patients’ inhaler techniques during consultations but 28.2(±19.1)% of patients were using their inhalers incorrectly; 21.1–57.9% of physicians could spot improper inhaler techniques in video demonstrations. And 79.6% of physicians believed combination inhalers could increase adherence because of convenience (53.7%), efficacy (52.7%) and usability (18.9%). Initial and follow-up consultations took 16.8(±8.4) and 9.2(±5.3) minutes, respectively. Most (85.1%) physicians used verbal conversations and least (24.5%), video demonstrations of inhaler use; 56.8% agreed that patient attitudes influenced their treatment approach. <i>Conclusion:</i> Physicians and patients have different views of ‘well-controlled’ asthma. Although physicians informed patients about asthma and inhaler usage, they overestimated actual usage and patients’ knowledge was sub-optimal. Physician-patient interactions can be augmented with understanding of patient attitudes, visual aids and ancillary support to perform physical demonstrations to improve treatment outcomes.
DOI: 10.6084/m9.figshare.3187583
title: PP2A regulates kinetochore-microtubule attachment during meiosis I in oocyte

description: Studies using <i>in vitro</i> cultured oocytes have indicated that the protein phosphatase 2A (PP2A), a major serine/threonine protein phosphatase, participates in multiple steps of meiosis. Details of oocyte maturation regulation by PP2A remain unclear and an <i>in vivo</i> model can provide more convincing information. Here, we inactivated PP2A by mutating genes encoding for its catalytic subunits (PP2Acs) in mouse oocytes. We found that eliminating both PP2Acs caused female infertility. Oocytes lacking PP2Acs failed to complete 1<sup>st</sup> meiotic division due to chromosome misalignment and abnormal spindle assembly. In mitosis, PP2A counteracts Aurora kinase B/C (AurkB/C) to facilitate correct kinetochore-microtubule (KT-MT) attachment. In meiosis I in oocyte, we found that PP2Ac deficiency destabilized KT-MT attachments. Chemical inhibition of AurkB/C in PP2Ac-null oocytes partly restored the formation of lateral/merotelic KT-MT attachments but not correct KT-MT attachments. Taken together, our findings demonstrate that PP2Acs are essential for chromosome alignments and regulate the formation of correct KT-MT attachments in meiosis I in oocytes.
DOI: 10.6084/m9.figshare.3187583.v1
title: PP2A regulates kinetochore-microtubule attachment during meiosis I in oocyte

description: Studies using <i>in vitro</i> cultured oocytes have indicated that the protein phosphatase 2A (PP2A), a major serine/threonine protein phosphatase, participates in multiple steps of meiosis. Details of oocyte maturation regulation by PP2A remain unclear and an <i>in vivo</i> model can provide more convincing information. Here, we inactivated PP2A by mutating genes encoding for its catalytic subunits (PP2Acs) in mouse oocytes. We found that eliminating both PP2Acs caused female infertility. Oocytes lacking PP2Acs failed to complete 1<sup>st</sup> meiotic division due to chromosome misalignment and abnormal spindle assembly. In mitosis, PP2A counteracts Aurora kinase B/C (AurkB/C) to facilitate correct kinetochore-microtubule (KT-MT) attachment. In meiosis I in oocyte, we found that PP2Ac deficiency destabilized KT-MT attachments. Chemical inhibition of AurkB/C in PP2Ac-null oocytes partly restored the formation of lateral/merotelic KT-MT attachments but not correct KT-MT attachments. Taken together, our findings demonstrate that PP2Acs are essential for chromosome alignments and regulate the formation of correct KT-MT attachments in meiosis I in oocytes.
DOI: 10.6084/m9.figshare.3187587
title: Dual role of Med12 in PRC1-dependent gene repression and ncRNA-mediated transcriptional activation

description: Mediator is considered an enhancer of RNA-Polymerase II dependent transcription but its function and regulation in pluripotent mouse embryonic stem cells (mESCs) remains unresolved. One means of controlling the function of Mediator is provided by the binding of the Cdk8 module (Med12, Cdk8, Ccnc and Med13) to the core Mediator. Here we report that Med12 operates together with PRC1 to silence key developmental genes in pluripotency. At the molecular level, while PRC1 represses genes it is also required to assemble ncRNA containing Med12-Mediator complexes. In the course of cellular differentiation the H2A ubiquitin binding protein Zrf1 abrogates PRC1-Med12 binding and facilitates the association of Cdk8 with Mediator. This remodeling of Mediator-associated protein complexes converts Mediator from a transcriptional repressor to a transcriptional enhancer, which then mediates ncRNA-dependent activation of Polycomb target genes. Altogether, our data reveal how the interplay of PRC1, ncRNA and Mediator complexes controls pluripotency and cellular differentiation.
DOI: 10.6084/m9.figshare.3187587.v2
title: Dual role of Med12 in PRC1-dependent gene repression and ncRNA-mediated transcriptional activation

description: Mediator is considered an enhancer of RNA-Polymerase II dependent transcription but its function and regulation in pluripotent mouse embryonic stem cells (mESCs) remains unresolved. One means of controlling the function of Mediator is provided by the binding of the Cdk8 module (Med12, Cdk8, Ccnc and Med13) to the core Mediator. Here we report that Med12 operates together with PRC1 to silence key developmental genes in pluripotency. At the molecular level, while PRC1 represses genes it is also required to assemble ncRNA containing Med12-Mediator complexes. In the course of cellular differentiation the H2A ubiquitin binding protein Zrf1 abrogates PRC1-Med12 binding and facilitates the association of Cdk8 with Mediator. This remodeling of Mediator-associated protein complexes converts Mediator from a transcriptional repressor to a transcriptional enhancer, which then mediates ncRNA-dependent activation of Polycomb target genes. Altogether, our data reveal how the interplay of PRC1, ncRNA and Mediator complexes controls pluripotency and cellular differentiation.
DOI: 10.6084/m9.figshare.3187581
title: Deoxycholic acid (DCA) confers an intestinal phenotype on esophageal squamous epithelium via induction of the stemness-associated reprogramming factors OCT4 and SOX2

description: Barrett's esophagus (BE) is essentially a metaplasia in which the normal stratified squamous epithelium is replaced by columnar epithelium. This study focuses on the involvement of OCT4 and SOX2, 2 key cell-reprogramming factors, in the deoxycholic acid (DCA)-induced expression of the intestinal hallmarks Cdx2 and MUC2 using both in vivo and in vitro models. Up-regulated expression of OCT4 and down-regulated expression of SOX2 were observed in BE compared with normal esophagus and esophagitis. Consistent with the data in vivo, DCA induced time-dependent expression of OCT4 at both the mRNA and protein levels and decreased nuclear expression of SOX2 in Het-1A cells. Down-regulation of OCT4 expression by siRNA abrogated DCA-induced expression of Cdx2 and MUC2, whereas siRNA against SOX2 significantly upregulated the expression of both Cdx2 and MUC2. Our data indicate that both OCT4 and SOX2 play important roles in the development of BE triggered by bile acid reflux.
DOI: 10.6084/m9.figshare.3187581.v1
title: Deoxycholic acid (DCA) confers an intestinal phenotype on esophageal squamous epithelium via induction of the stemness-associated reprogramming factors OCT4 and SOX2

description: Barrett's esophagus (BE) is essentially a metaplasia in which the normal stratified squamous epithelium is replaced by columnar epithelium. This study focuses on the involvement of OCT4 and SOX2, 2 key cell-reprogramming factors, in the deoxycholic acid (DCA)-induced expression of the intestinal hallmarks Cdx2 and MUC2 using both in vivo and in vitro models. Up-regulated expression of OCT4 and down-regulated expression of SOX2 were observed in BE compared with normal esophagus and esophagitis. Consistent with the data in vivo, DCA induced time-dependent expression of OCT4 at both the mRNA and protein levels and decreased nuclear expression of SOX2 in Het-1A cells. Down-regulation of OCT4 expression by siRNA abrogated DCA-induced expression of Cdx2 and MUC2, whereas siRNA against SOX2 significantly upregulated the expression of both Cdx2 and MUC2. Our data indicate that both OCT4 and SOX2 play important roles in the development of BE triggered by bile acid reflux.
DOI: 10.6084/m9.figshare.3187587.v1
title: Dual Role of Med12 in PRC1-dependent Gene Repression and ncRNA-mediated Transcriptional Activation

description: Mediator is considered an enhancer of RNA-Polymerase II dependent transcription but its function and regulation in pluripotent mouse embryonic stem cells (mESCs) remains unresolved. One means of controlling the function of Mediator is provided by the binding of the Cdk8 module (Med12, Cdk8, Ccnc and Med13) to the core Mediator. Here we report that Med12 operates together with PRC1 to silence key developmental genes in pluripotency. At the molecular level, while PRC1 represses genes it is also required to assemble ncRNA containing Med12-Mediator complexes. In the course of cellular differentiation the H2A ubiquitin binding protein Zrf1 abrogates PRC1-Med12 binding and facilitates the association of Cdk8 with Mediator. This remodeling of Mediator-associated protein complexes converts Mediator from a transcriptional repressor to a transcriptional enhancer, which then mediates ncRNA-dependent activation of Polycomb target genes. Altogether, our data reveal how the interplay of PRC1, ncRNA and Mediator complexes controls pluripotency and cellular differentiation.
DOI: 10.6084/m9.figshare.3187575
title: Autophagy initiation correlates with the autophagic flux in 3D models of mesothelioma and with patient outcome

description: Understanding the role of autophagy in cancer has been limited by the inability to measure this dynamic process in formalin-fixed tissue. We considered that 3-dimensional models including ex vivo tumor, such as we have developed for studying mesothelioma, would provide valuable insights. Using these models, in which we could use lysosomal inhibitors to measure the autophagic flux, we sought a marker of autophagy that would be valid in formalin-fixed tumor and be used to assess the role of autophagy in patient outcome. Autophagy was studied in mesothelioma cell lines, as 2-dimensional (2D) monolayers and 3-dimensional (3D) multicellular spheroids (MCS), and in tumor from 25 chemonaive patients, both as ex vivo 3D tumor fragment spheroids (TFS) and as formalin-fixed tissue. Autophagy was evaluated as autophagic flux by detection of the accumulation of LC3 after lysosomal inhibition and as autophagy initiation by detection of ATG13 puncta. We found that autophagic flux in 3D, but not in 2D, correlated with ATG13 positivity. In each TFS, ATG13 positivity was similar to that of the original tumor. When tested in tissue microarrays of 109 chemonaive patients, higher ATG13 positivity correlated with better prognosis and provided information independent of known prognostic factors. Our results show that ATG13 is a static marker of the autophagic flux in 3D models of mesothelioma and may also reflect autophagy levels in formalin-fixed tumor. If confirmed, this marker would represent a novel prognostic factor for mesothelioma, supporting the notion that autophagy plays an important role in this cancer.
DOI: 10.6084/m9.figshare.3187571
title: NUP98 fusion oncoproteins interact with the APC/C<sup>Cdc20</sup> as a pseudosubstrate and prevent mitotic checkpoint complex binding

description: <i>NUP98</i> is a recurrent partner gene in translocations causing acute myeloid leukemias and myelodisplastic syndrome. The expression of NUP98 fusion oncoproteins has been shown to induce mitotic spindle defects and chromosome missegregation, which correlate with the capability of NUP98 fusions to cause mitotic checkpoint attenuation. We show that NUP98 oncoproteins physically interact with the APC/C<sup>Cdc20</sup> in the absence of the NUP98 partner protein RAE1, and prevent the binding of the mitotic checkpoint complex to the APC/C<sup>Cdc20</sup>. NUP98 oncoproteins require the GLEBS-like domain present in their NUP98 moiety to bind the APC/C<sup>Cdc20</sup>. We found that NUP98 wild-type is a substrate of APC/C<sup>Cdc20</sup> prior to mitotic entry, and that its binding to APC/C<sup>Cdc20</sup> is controlled via phosphorylation of a PEST sequence located within its C-terminal portion. We identify S606, within the PEST sequence, as a key target site, whose phosphorylation modulates the capability of NUP98 to interact with APC/C<sup>Cdc20</sup>. We finally provide evidence for an involvement of the peptidyl-prolyl isomerase PIN1 in modulating the possible conformational changes within NUP98 that lead to its dissociation from the APC/C<sup>Cdc20</sup> during mitosis. Our results provide novel insight into the mechanisms underlying the aberrant capability of NUP98 oncoproteins to interact with APC/C<sup>Cdc20</sup> and to interfere with its function.