cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5410729
title: G0S2 represses PI3K/mTOR signaling and increases sensitivity to PI3K/mTOR pathway inhibitors in breast cancer

description: G0/G1 switch gene 2 (G0S2) is a direct retinoic acid target implicated in cancer biology and therapy based on frequent methylation-mediated silencing in diverse solid tumors. We recently reported that low G0S2 expression in breast cancer, particularly estrogen receptor-positive (ER+) breast cancer, correlates with increased rates of recurrence, indicating that G0S2 plays a role in breast cancer progression. However, the function(s) and mechanism(s) of G0S2 tumor suppression remain unclear. In order to determine potential mechanisms of G0S2 anti-oncogenic activity, we performed genome-wide expression analysis that revealed an enrichment of gene signatures related to PI3K/mTOR pathway activation in G0S2 null cells as compared to G0S2 wild-type cells. G0S2 null cells also exhibited a dramatic decreased sensitivity to PI3K/mTOR pathway inhibitors. Conversely, restoring G0S2 expression in human ER+ breast cancer cells decreased basal mTOR signaling and sensitized the cells to pharmacologic mTOR pathway inhibitors. Notably, we provide evidence here that the increase in recurrence seen with low G0S2 expression is especially prominent in patients who have undergone antiestrogen therapy. Further, ER+ breast cancer cells with restored G0S2 expression had a relative increased sensitivity to tamoxifen. These findings reveal that in breast cancer G0S2 functions as a tumor suppressor in part by repressing PI3K/mTOR activity, and that G0S2 enhances therapeutic responses to PI3K/mTOR inhibitors. Recent studies implicate hyperactivation of PI3K/mTOR signaling as promoting resistance to antiestrogen therapies in ER+ breast cancer. Our data establishes G0S2 as opposing this form of antiestrogen resistance. This promotes further investigation of the role of G0S2 as an antineoplastic breast cancer target and a biomarker for recurrence and therapy response.
DOI: 10.6084/m9.figshare.5410726.v1
title: Factors that influence tear meniscus area and conjunctivochalasis: The Singapore Indian eye study

description: <b><i>Purpose</i></b>: Assessment of tear film and conjunctiva is critical to define presence and severity of ocular surface disease. We aimed to characterize tear meniscus area (TMA) and conjunctivochalasis by anterior segment optical coherence tomography (ASOCT) in population-based patients and identify potential factors associated with low TMA and severe conjunctivochalasis. <b><i>Methods</i></b>: Study subjects were enrolled from The Singapore Indian Eye Study, a population-based study of Asian Indian in Singapore. Imaging with ASOCT was performed on three ocular regions (nasal, central and temporal). TMA was obtained by measuring the cross-sectional area of the inferior tear meniscus. Severity of conjunctivochalasis was quantified by measuring the conjunctivochalasis ratio (CCR), the ratio of area of redundant conjunctiva to the TMA. Ocular symptoms and demographic factors were assessed by standardized questionnaires. <b><i>Results</i></b>: A total of 403 participants (52.9% women) 40 years of age and older were included. TMA centrally was 2818 ± 5308 pixel<sup>2</sup>. Female sex and the presence of meibomian gland dysfunction (MGD), but not older age, were associated with a lower TMA (p = 0.031, p = 0.031 and p = 0.956 respectively). In this population, 9.2% had severe conjunctivochalasis (CCR&gt;0.7) whereas 39.0% had mild to no conjunctivochalasis (CCR≤0.3). Conjunctivochalasis was more severe in temporal, followed by nasal and central sections. Older age was associated with severe conjunctivochalasis (p <b><i>Conclusion</i></b>: MGD and female gender were associated with lower TMA, while older age was associated with increased severity of conjunctivochalasis. Objective measurement of TMA and CCR using ASOCT imaging may be useful in the assessment of tear volume and ocular surface tear function.
DOI: 10.6084/m9.figshare.5410729.v1
title: G0S2 represses PI3K/mTOR signaling and increases sensitivity to PI3K/mTOR pathway inhibitors in breast cancer

description: G0/G1 switch gene 2 (G0S2) is a direct retinoic acid target implicated in cancer biology and therapy based on frequent methylation-mediated silencing in diverse solid tumors. We recently reported that low G0S2 expression in breast cancer, particularly estrogen receptor-positive (ER+) breast cancer, correlates with increased rates of recurrence, indicating that G0S2 plays a role in breast cancer progression. However, the function(s) and mechanism(s) of G0S2 tumor suppression remain unclear. In order to determine potential mechanisms of G0S2 anti-oncogenic activity, we performed genome-wide expression analysis that revealed an enrichment of gene signatures related to PI3K/mTOR pathway activation in G0S2 null cells as compared to G0S2 wild-type cells. G0S2 null cells also exhibited a dramatic decreased sensitivity to PI3K/mTOR pathway inhibitors. Conversely, restoring G0S2 expression in human ER+ breast cancer cells decreased basal mTOR signaling and sensitized the cells to pharmacologic mTOR pathway inhibitors. Notably, we provide evidence here that the increase in recurrence seen with low G0S2 expression is especially prominent in patients who have undergone antiestrogen therapy. Further, ER+ breast cancer cells with restored G0S2 expression had a relative increased sensitivity to tamoxifen. These findings reveal that in breast cancer G0S2 functions as a tumor suppressor in part by repressing PI3K/mTOR activity, and that G0S2 enhances therapeutic responses to PI3K/mTOR inhibitors. Recent studies implicate hyperactivation of PI3K/mTOR signaling as promoting resistance to antiestrogen therapies in ER+ breast cancer. Our data establishes G0S2 as opposing this form of antiestrogen resistance. This promotes further investigation of the role of G0S2 as an antineoplastic breast cancer target and a biomarker for recurrence and therapy response.
DOI: 10.6084/m9.figshare.5410525
title: Papers, Tweets, and Facebook posts about Zika

description: Data corresponding to the submission: Local chatter or international buzz? Language differences on posts about short title: Zika research on Twitter and Facebook
DOI: 10.6084/m9.figshare.5409550
title: SidePak Flow Rate Calculation

description: Flow rate calculations for SidePak.
DOI: 10.6084/m9.figshare.5409550.v1
title: SidePak Flow Rate Calculation

description: Flow rate calculations for SidePak.
DOI: 10.6084/m9.figshare.5406787
title: Succinic acid treatment of SCA1 transgenic mice

description: Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved behavior. Thus, treatment with succinic acid shows promise as a therapeutic adjuvant in neurodegenerative ataxias, and warrants further investigation. <b><br></b><b>All data from this manuscript will be made available upon acceptance by PLoS One.</b>
DOI: 10.6084/m9.figshare.5406799
title: Afghanistan 3W supply dataset for the first trimester of 2015.

description: Afghanistan 3W supply dataset for the first trimester of 2015.
DOI: 10.6084/m9.figshare.5406799.v1
title: Supply dataset

description: Afghanistan 3W supply dataset for the first trimester of 2015.
DOI: 10.6084/m9.figshare.5406718
title: GY63 daytime song

description: raw data files - ch1 air sac pressrue, ch2 emg 1; ch3 emg 2; ch4 mic
DOI: 10.6084/m9.figshare.5406718.v1
title: GY63 daytime song

description: raw data files - ch1 air sac pressrue, ch2 emg 1; ch3 emg 2; ch4 mic
DOI: 10.6084/m9.figshare.5406787.v1
title: Succinica acid treatment of SCA1 transgenic mice

description: Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved behavior. Thus, treatment with succinic acid shows promise as a therapeutic adjuvant in neurodegenerative ataxias, and warrants further investigation. <b><br></b><b>All data from this manuscript will be made available upon acceptance by PLoS One.</b>
DOI: 10.6084/m9.figshare.5406733.v1
title: Supplementary data for Shakya et al. (2017)

description: This data set contains sequences, sequence alignments and phylogenetic trees used in the bioinformatic analyses presented in:<br><br>Shakya M, Soucy SM, and Zhaxybayeva O. "Insights into Origin and Evolution of α-proteobacterial Gene Transfer Agents", submitted. <br><br><b>File Contents:<br><br></b><b></b><b>RefSeq_bacterial_hits.zip:</b> FASTA-formatted files of detected bacterial homologs of RcGTA genes in RefSeq database release 76. The filenames correspond to gene names listed in Supplementary Table S4. <b>RefSeq_viral_hits.zip:</b> FASTA-formatted files of detected viral homologs of RcGTA genes within RefSeq database release 76. The filenames correspond to gene names listed in Supplementary Table S4. <br> <b>GTA_Rhodobacterales_queries.zip</b>: FASTA-formatted files of RcGTA homologs from <i>Rhodobacterales</i> that were used in BLAST searches of <i>RefSeq</i> database and 255 α-proteobacterial genomes. <br> <b>individual_proteins.zip</b>: FASTA-formatted alignments of individual RcGTA structural cluster genes and their large cluster (LC) homologs used to create the LC-locus alignment. The filenames correspond to gene names listed in Supplementary Table S4. <br><b>individual_trees.zip</b>: NEWICK-formatted phylogenetic trees reconstructed from the alignments in individual_protein.zip file. These trees were used in analyses shown in Supplementary Table S3. <b>LC_locus.zip</b>: FASTA-formatted LC-locus alignment and NEWICK-formatted phylogenetic tree of the LC-locus (the right panel of Figure 6). <br> <b>flanking_genes.zip</b>: FASTA-formatted alignments and NEWICK-formatted phylogenetic trees of three genes that were found flanking large clusters detected in non-alpha-proteobacterial genomes. The trees are shown in Supplementary Figure S8. <b>PPD.zip: </b> Pairwise phylogenetic distances (PPDs) of RcGTA homologs found in large clusters (LC), small clusters (SC), and viruses in tab-delimited text files, and FASTA-formatted alignments of RcGTA homologs used to calculate the PPDs. The data are shown in Supplementary Figure S4. <b>reference_tree.zip: </b>PHYLIP-formatted<b> </b>concatenated alignment of 99 alignments of genes conserved across<b> </b>α-proteobacteria (see Supplementary Table S2), and NEWICK-formatted phylogenetic trees reconstructed using this alignment (see Figure 6 and Supplementary Figure S3.) <b>StructuralClusterHomologs.xlsx: </b>An Excel spreadsheet with information about RcGTA homologs found in small clusters (SC) and large clusters (LC) across alpha-proteobacterial genomes. The table contains the GI numbers of each homologs, as well as accession number and taxonomic information of the source genome. <b> </b>
DOI: 10.6084/m9.figshare.5406787.v2
title: Succinic acid treatment of SCA1 transgenic mice

description: Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved behavior. Thus, treatment with succinic acid shows promise as a therapeutic adjuvant in neurodegenerative ataxias, and warrants further investigation. <b><br></b><b>All data from this manuscript will be made available upon acceptance by PLoS One.</b>
DOI: 10.6084/m9.figshare.5406628
title: Individual CMR and BCI data from Fragile co-existence of a global chytrid pathogen with amphibian populations is mediated by environment and demography

description: Capture-recapture data per individual toad per site visit and the associated data on the body condition of each individual toad upon capture
DOI: 10.6084/m9.figshare.5406628.v1
title: Individual CMR and BCI data from Fragile co-existence of a global chytrid pathogen with amphibian populations is mediated by environment and demography

description: Capture-recapture data per individual toad per site visit and the associated data on the body condition of each individual toad upon capture
DOI: 10.6084/m9.figshare.5406613
title: Table S4 from Persistent and plastic effects of temperature on DNA methylation across the genome of threespine stickleback (<i>Gasterosteus aculeatus</i>)

description: Annotated genes associated with differentially methylated regions
DOI: 10.6084/m9.figshare.5406787.v4
title: Succinic acid treatment of SCA1 transgenic mice

description: Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved behavior. Thus, treatment with succinic acid shows promise as a therapeutic adjuvant in neurodegenerative ataxias, and warrants further investigation. <b><br></b><b>All data from this manuscript will be made available upon acceptance by PLoS One.</b>
DOI: 10.6084/m9.figshare.5406604
title: Annual counts of juvenile toads from Fragile co-existence of a global chytrid pathogen with amphibian populations is mediated by environment and demography

description: Total counts of juvenile Bombina variegata per site per year
DOI: 10.6084/m9.figshare.5406604.v1
title: Annual counts of juvenile toads from Fragile co-existence of a global chytrid pathogen with amphibian populations is mediated by environment and demography

description: Total counts of juvenile Bombina variegata per site per year
DOI: 10.6084/m9.figshare.5406787.v5
title: Succinic acid treatment of SCA1 transgenic mice

description: Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved behavior. Thus, treatment with succinic acid shows promise as a therapeutic adjuvant in neurodegenerative ataxias, and warrants further investigation. <b><br></b><b>All data from this manuscript will be made available upon acceptance by PLoS One.</b>
DOI: 10.6084/m9.figshare.5406787.v6
title: Succinic acid treatment of SCA1 transgenic mice

description: Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved behavior. Thus, treatment with succinic acid shows promise as a therapeutic adjuvant in neurodegenerative ataxias, and warrants further investigation. <b><br></b><b>All data from this manuscript will be made available upon acceptance by PLoS One.</b>
DOI: 10.6084/m9.figshare.5406586
title: Table S1 from Identifying the most surprising victims of mass extinction events: an example using Late Ordovician Brachiopods

description: Genus name, status (extinct by the end of interval or survives into the next interval) and risk preditions from all five background intervals for all genera in the latest Katian (Katian 4) and Hirnantian.
DOI: 10.6084/m9.figshare.5406589
title: Sample code and data from Feeding the world's largest fish: highly variable whale shark residency patterns at a provisioning site in the Philippines

description: Sample R code used to run permutation tests and PCoA to categorize whale shark residency patterns at the provisioning site. Data provided are three years of daily presence-absence data for Y1 ID frequent sharks (refer to manuscript)
DOI: 10.6084/m9.figshare.5406787.v7
title: Succinic acid treatment of SCA1 transgenic mice

description: Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved behavior. Thus, treatment with succinic acid shows promise as a therapeutic adjuvant in neurodegenerative ataxias, and warrants further investigation. <b><br></b><b>All data from this manuscript will be made available upon acceptance by PLoS One.</b>
DOI: 10.6084/m9.figshare.5406583
title: Data from Age-dependent associations between telomere length and environmental conditions in roe deer

description: Data used in manuscript
DOI: 10.6084/m9.figshare.5406586.v1
title: Table S1 from Identifying the most surprising victims of mass extinction events: an example using Late Ordovician Brachiopods

description: Genus name, status (extinct by the end of interval or survives into the next interval) and risk preditions from all five background intervals for all genera in the latest Katian (Katian 4) and Hirnantian.
DOI: 10.6084/m9.figshare.5406589.v1
title: Sample code and data from Feeding the world's largest fish: highly variable whale shark residency patterns at a provisioning site in the Philippines

description: Sample R code used to run permutation tests and PCoA to categorize whale shark residency patterns at the provisioning site. Data provided are three years of daily presence-absence data for Y1 ID frequent sharks (refer to manuscript)
DOI: 10.6084/m9.figshare.5406583.v1
title: Data from Age-dependent associations between telomere length and environmental conditions in roe deer

description: Data used in manuscript
DOI: 10.6084/m9.figshare.5406526
title: Lightrail

description: Data collected from light rail passengers.
DOI: 10.6084/m9.figshare.5406532
title: Walking

description: Data collected from walkers.
DOI: 10.6084/m9.figshare.5406526.v1
title: Lightrail

description: Data collected from light rail passengers.
DOI: 10.6084/m9.figshare.5406532.v1
title: Walking

description: Data collected from walkers.