cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3365335
title: Sharpe_PreySizeCompetition.csv

description: There are many benefits of group living, but also substantial costs, one of which is competition for resources. How scarce food resources are distributed among different members of a population or social group—whether via scramble or contest competition— can influence not only the variance in individual fitness, but also the stability and therefore survival of the group or population. 2. Attributes of the food resources themselves, such as their size, may also influence the type of intraspecific competition that occurs, and therefore the intrinsic stability of a group or population. 3. By experimentally manipulating the size of prey fed to artificial colonies of the social spider <i>Anelosimus eximius, </i>we investigated whether prey size could alter the degree of scramble vs. contest competition that takes place and, thus, potentially, influence colony population dynamics. 4. We found that large prey were shared more evenly than small prey, and that individuals in poor condition were more likely to feed when prey were large than when prey were small. Additionally we show that individuals participating in prey capture are also more likely to feed on the captured prey. 5. We developed a simple mathematical model to explore the prey sizes that would be energetically worth defending, i.e. “economically defendable”. The model shows that neither very small, nor prey above a certain size is worth monopolizing 6. As the size of prey captured by social spider colonies increases with colony size, our findings suggest that scramble competition may predominate in large colonies. Scramble competition, combined with the fact that prey biomass per capita declines as colonies grow beyond a certain size, would then explain why extremely large colonies of this social spider may suddenly go extinct. Our project thus illustrates the potential triple link between characteristics of the resources, individual behaviour, and population dynamics, a link rarely considered in an empirical setting.
DOI: 10.6084/m9.figshare.3365326
title: Supplmentary Table S1

description: List of publicly available Staphylococcus epidermidis genomes used in this study
DOI: 10.6084/m9.figshare.3365326.v1
title: Supplmentary Table S1

description: List of publicly available Staphylococcus epidermidis genomes used in this study
DOI: 10.6084/m9.figshare.3365317
title: data systematic review Weidlich et al..xlsx

description: Dataset of articles included in the meta-analysis entitled "Association between metabolic syndrome and periodontitis: a systematic review and meta-analysis". <b></b><b></b>
DOI: 10.6084/m9.figshare.3365317.v1
title: data systematic review Weidlich et al..xlsx

description: Dataset of articles included in the meta-analysis entitled "Association between metabolic syndrome and periodontitis: a systematic review and meta-analysis". <b></b><b></b>
DOI: 10.6084/m9.figshare.3365299
title: Data and Alignment Files for Baltrus et al. AmrZ Manuscript

description: An Excel spreadsheet containing data from motility assays and in<i> Pseudomonas stutzeri </i>focused on <i>amrZ</i> deletion strains and complements. <br>Alignments used to build Bayesian phylogenies for RpoD/GyrB and AmrZ
DOI: 10.6084/m9.figshare.3365299.v1
title: Motility data for amrZ strains

description: Raw data from motility assays in<i> Pseudomonas stutzeri </i>focused on <i>amrZ</i> deletion strains and complements
DOI: 10.6084/m9.figshare.3365299.v2
title: Motility data for amrZ strains

description: Raw data from motility assays in<i> Pseudomonas stutzeri </i>focused on <i>amrZ</i> deletion strains and complements
DOI: 10.6084/m9.figshare.3365299.v4
title: Data and Alignment Files for Baltrus et al. AmrZ Manuscript

description: An Excel spreadsheet containing data from motility assays and in<i> Pseudomonas stutzeri </i>focused on <i>amrZ</i> deletion strains and complements. <br>Alignments used to build Bayesian phylogenies for RpoD/GyrB and AmrZ
DOI: 10.6084/m9.figshare.3365299.v3
title: Motility and colony spreading Data for amrZ strains as well as protein alignments used to build phylogenies

description: An Excel spreadsheet containing data from motility assays and in<i> Pseudomonas stutzeri </i>focused on <i>amrZ</i> deletion strains and complements. <br>Alignments used to build Bayesian phylogenies for RpoD/GyrB and AmrZ
DOI: 10.6084/m9.figshare.3365293
title: Hylawrightorum_HuachucaMountains_Mimsetal.xlsx

description: Genotype data for 17 microsatellite loci for the species <i>Hyla wrightorum</i>. Please see Mims et al. (in revision, PLOS ONE) for details on methods.
DOI: 10.6084/m9.figshare.3365293.v1
title: FigShare.xlsx

description: Genotype data for 17 microsatellite loci for the species <i>Hyla wrightorum</i>. Please see Mims et al. (in revision, PLOS ONE) for details on methods.
DOI: 10.6084/m9.figshare.3365293.v3
title: Hylawrightorum_HuachucaMountains_Mimsetal.xlsx

description: Genotype data for 17 microsatellite loci for the species <i>Hyla wrightorum</i>. Please see Mims et al. (in revision, PLOS ONE) for details on methods.
DOI: 10.6084/m9.figshare.3365293.v2
title: FigShare.xlsx

description: Genotype data for 17 microsatellite loci for the species <i>Hyla wrightorum</i>. Please see Mims et al. (in revision, PLOS ONE) for details on methods.
DOI: 10.5281/zenodo.4014965
title: Marilao, Bulacan Population Projection from 2020 to 2100

description: Computation of Marilao, Bulacan Population Projection from 2020 to 2100
DOI: 10.6084/m9.figshare.3365263
title: amrZ gene complements for P. stutzeri

description: Overview of how constructs for complementation of an <i>amrZ</i> mutant in <i>P. stutzeri w</i>ere created
DOI: 10.6084/m9.figshare.3365263.v1
title: amrZ gene complements for P. stutzeri

description: Overview of how constructs for complementation of an <i>amrZ</i> mutant in <i>P. stutzeri w</i>ere created
DOI: 10.6084/m9.figshare.3365005
title: LEDs_spectrum.csv

description: This dataset contains the spectrum of lights used for the five-primary system in the experiments reported by Barrionuevo & Cao in the manuscript "Luminance and chromatic signals interact differently with melanopsin activation to control the pupil light response". This data show the spectral characteristics of the light sources used at 20% of the maximum output.
DOI: 10.6084/m9.figshare.3364903
title: Metformin inhibits proliferation and migration of glioblastoma cells independently of TGF-β2

description: To this day, glioblastoma (GBM) remains an incurable brain tumor. Previous research has shown that metformin, an oral anti-diabetic drug, may decrease GBM cell proliferation and migration especially in brain tumor initiating cells (BTICs). As transforming growth factor β 2 (TGF-β<sub>2</sub>) has been reported to promote high-grade glioma and is inhibited by metformin in other tumors, we explored whether metformin directly interferes with TGF-β<sub>2</sub>-signaling. Functional investigation of proliferation and migration of primary BTICs after treatment with metformin+/−TGF-β<sub>2</sub> revealed that metformin doses as low as 0.01 mM metformin thrice a day were able to inhibit proliferation of susceptible cell lines, whereas migration was impacted only at higher doses. Known cellular mechanisms of metformin, such as increased lactate secretion, reduced oxygen consumption and activated AMPK-signaling, could be confirmed. However, TGF-β<sub>2</sub> and metformin did not act as functional antagonists, but both rather inhibited proliferation and/or migration, if significant effects were present. We did not observe a relevant influence of metformin on TGF-β<sub>2</sub> mRNA expression (qRT-PCR), TGF-β<sub>2</sub> protein expression (ELISA) or SMAD-signaling (Western blot). Therefore, it seems that metformin does not exert its inhibitory effects on GBM BTIC proliferation and migration by altering TGF-β<sub>2</sub>-signaling. Nonetheless, as low doses of metformin are able to reduce proliferation of certain GBM cells, further exploration of predictors of BTICs' susceptibility to metformin appears justified.
DOI: 10.6084/m9.figshare.3364903.v2
title: Metformin inhibits proliferation and migration of glioblastoma cells independently of TGF-β2

description: To this day, glioblastoma (GBM) remains an incurable brain tumor. Previous research has shown that metformin, an oral anti-diabetic drug, may decrease GBM cell proliferation and migration especially in brain tumor initiating cells (BTICs). As transforming growth factor β 2 (TGF-β<sub>2</sub>) has been reported to promote high-grade glioma and is inhibited by metformin in other tumors, we explored whether metformin directly interferes with TGF-β<sub>2</sub>-signaling. Functional investigation of proliferation and migration of primary BTICs after treatment with metformin+/−TGF-β<sub>2</sub> revealed that metformin doses as low as 0.01 mM metformin thrice a day were able to inhibit proliferation of susceptible cell lines, whereas migration was impacted only at higher doses. Known cellular mechanisms of metformin, such as increased lactate secretion, reduced oxygen consumption and activated AMPK-signaling, could be confirmed. However, TGF-β<sub>2</sub> and metformin did not act as functional antagonists, but both rather inhibited proliferation and/or migration, if significant effects were present. We did not observe a relevant influence of metformin on TGF-β<sub>2</sub> mRNA expression (qRT-PCR), TGF-β<sub>2</sub> protein expression (ELISA) or SMAD-signaling (Western blot). Therefore, it seems that metformin does not exert its inhibitory effects on GBM BTIC proliferation and migration by altering TGF-β<sub>2</sub>-signaling. Nonetheless, as low doses of metformin are able to reduce proliferation of certain GBM cells, further exploration of predictors of BTICs' susceptibility to metformin appears justified.
DOI: 10.6084/m9.figshare.3364903.v1
title: Metformin inhibits proliferation and migration of glioblastoma cells independently of TGF-β2

description: To this day, glioblastoma (GBM) remains an incurable brain tumor. Previous research has shown that metformin, an oral anti-diabetic drug, may decrease GBM cell proliferation and migration especially in brain tumor initiating cells (BTICs). As transforming growth factor beta 2 (TGF-β<sub>2</sub>) has been reported to promote high-grade glioma and is inhibited by metformin in other tumors, we explored whether metformin directly interferes with TGF-β<sub>2</sub>-signaling. Functional investigation of proliferation and migration of primary BTICs after treatment with metformin+/−TGF-β<sub>2</sub> revealed that metformin doses as low as 0.01 mM metformin thrice a day were able to inhibit proliferation of susceptible cell lines, whereas migration was impacted only at higher doses. Known cellular mechanisms of metformin, such as increased lactate secretion, reduced oxygen consumption and activated AMPK-signaling, could be confirmed. However, TGF-β<sub>2</sub> and metformin did not act as functional antagonists, but both rather inhibited proliferation and/or migration, if significant effects were present. We did not observe a relevant influence of metformin on TGF-β<sub>2</sub> mRNA expression (qRT-PCR), TGF-β<sub>2</sub> protein expression (ELISA) or SMAD-signaling (Western blot). Therefore, it seems that metformin does not exert its inhibitory effects on GBM BTIC proliferation and migration by altering TGF-β<sub>2</sub>-signaling. Nonetheless, as low doses of metformin are able to reduce proliferation of certain GBM cells, further exploration of predictors of BTICs' susceptibility to metformin appears justified.
DOI: 10.6084/m9.figshare.3364900
title: A novel tumor-promoting mechanism of IL6 and the therapeutic efficacy of tocilizumab: Hypoxia-induced IL6 is a potent autophagy initiator in glioblastoma via the p-STAT3-<i>MIR155-3p</i>-CREBRF pathway

description: Hypoxia induces protective autophagy in glioblastoma cells and new therapeutic avenues that target this process may improve the outcome for glioblastoma patients. Recent studies have suggested that the autophagic process is upregulated in glioblastomas in response to extensive hypoxia. Hypoxia also induces the upregulation of a specific set of proteins and microRNAs (miRNAs) in a variety of cell types. IL6 (interleukin 6), an inflammatory autocrine and paracrine cytokine that is overexpressed in glioblastoma, has been reported to be a biomarker for poor prognosis because of its tumor-promoting effects. Here, we describe a novel tumor-promoting mechanism of IL6, whereby hypoxia-induced IL6 acts as a potent initiator of autophagy in glioblastoma via the phosphorylated (p)-STAT3-<i>MIR155-3p</i> pathway. IL6 and p-STAT3 levels correlated with the abundance of autophagic cells and HIF1A levels in human glioma tissues and with the grade of human glioma, whereas inhibition of exogenous or endogenous IL6 repressed autophagy in glioblastoma cells in vitro. Knockdown of endogenous <i>MIR155-3p</i> inhibited IL6-induced autophagy, and enforced expression of <i>MIR155-3p</i> restored the anti-autophagic activity of IL6 inhibitors. We show that the hypoxia-IL6-p-STAT3-<i>MIR155-3p</i>-CREBRF-CREB3-ATG5 pathway plays a central role in malignant glioma progression, with blockade of the IL6 receptor by tocilizumab demonstrating a certain level of therapeutic efficacy in a xenograft model in vivo, especially in combination with temozolomide. Moreover, tocilizumab inhibits autophagy by promoting tumor apoptosis. Collectively, our findings provide new insight into the molecular mechanisms underlying hypoxia-induced glioma cell autophagy and point toward a possible efficacious adjuvant therapy for glioblastoma patients.
DOI: 10.6084/m9.figshare.3364900.v2
title: A novel tumor-promoting mechanism of IL6 and the therapeutic efficacy of tocilizumab: Hypoxia-induced IL6 is a potent autophagy initiator in glioblastoma via the p-STAT3-<i>MIR155-3p</i>-CREBRF pathway

description: Hypoxia induces protective autophagy in glioblastoma cells and new therapeutic avenues that target this process may improve the outcome for glioblastoma patients. Recent studies have suggested that the autophagic process is upregulated in glioblastomas in response to extensive hypoxia. Hypoxia also induces the upregulation of a specific set of proteins and microRNAs (miRNAs) in a variety of cell types. IL6 (interleukin 6), an inflammatory autocrine and paracrine cytokine that is overexpressed in glioblastoma, has been reported to be a biomarker for poor prognosis because of its tumor-promoting effects. Here, we describe a novel tumor-promoting mechanism of IL6, whereby hypoxia-induced IL6 acts as a potent initiator of autophagy in glioblastoma via the phosphorylated (p)-STAT3-<i>MIR155-3p</i> pathway. IL6 and p-STAT3 levels correlated with the abundance of autophagic cells and HIF1A levels in human glioma tissues and with the grade of human glioma, whereas inhibition of exogenous or endogenous IL6 repressed autophagy in glioblastoma cells in vitro. Knockdown of endogenous <i>MIR155-3p</i> inhibited IL6-induced autophagy, and enforced expression of <i>MIR155-3p</i> restored the anti-autophagic activity of IL6 inhibitors. We show that the hypoxia-IL6-p-STAT3-<i>MIR155-3p</i>-CREBRF-CREB3-ATG5 pathway plays a central role in malignant glioma progression, with blockade of the IL6 receptor by tocilizumab demonstrating a certain level of therapeutic efficacy in a xenograft model in vivo, especially in combination with temozolomide. Moreover, tocilizumab inhibits autophagy by promoting tumor apoptosis. Collectively, our findings provide new insight into the molecular mechanisms underlying hypoxia-induced glioma cell autophagy and point toward a possible efficacious adjuvant therapy for glioblastoma patients.
DOI: 10.6084/m9.figshare.3364900.v1
title: A Novel Tumor-promoting Mechanism of IL6 and the Therapeutic Efficacy of Tocilizumab: Hypoxia-induced IL6 Is a Potent Autophagy Initiator in Glioblastoma via the p-STAT3-<i>MIR155-3p</i>-CREBRF Pathway

description: Hypoxia induces protective autophagy in glioblastoma cells, and new therapeutic avenues that target this process may improve the outcome for glioblastoma patients. Recent studies have suggested that the autophagic process is upregulated in glioblastomas in response to extensive hypoxia. Hypoxia also induces the upregulation of a specific set of proteins and microRNAs (miRNAs) in a variety of cell types. IL6 (interleukin 6), an inflammatory autocrine and paracrine cytokine that is overexpressed in glioblastoma, has been reported to be a biomarker for poor prognosis because of its tumor-promoting effects. Here, we describe a novel tumor-promoting mechanism of IL6, whereby hypoxia-induced IL6 acts as a potent initiator of autophagy in glioblastoma via the phosphorylated (p)-STAT3-<i>MIR155-3p</i> pathway. IL6 and p-STAT3 levels correlated with the abundance of autophagic cells and HIF1A levels in human glioma tissues and with the grade of human glioma, whereas inhibition of exogenous or endogenous IL6 repressed autophagy in glioblastoma cells in vitro. Knockdown of endogenous <i>MIR155-3p</i> inhibited IL6-induced autophagy, and enforced expression of <i>MIR155-3p</i> restored the anti-autophagic activity of IL6 inhibitors. We show that the hypoxia-IL6-p-STAT3-<i>MIR155-3p</i>-CREBRF-CREB3-ATG5 pathway plays a central role in malignant glioma progression, with blockade of the IL6 receptor by tocilizumab demonstrating a certain level of therapeutic efficacy in a xenograft model in vivo, especially in combination with temozolomide. Moreover, tocilizumab inhibits autophagy by promoting tumor apoptosis. Collectively, our findings provide new insight into the molecular mechanisms underlying hypoxia-induced glioma cell autophagy and point toward a possible efficacious adjuvant therapy for glioblastoma patients.
DOI: 10.6084/m9.figshare.3364894
title: Negative control of CSL gene transcription by stress/DNA damage response and p53

description: CSL is a key transcriptional repressor and mediator of Notch signaling. Despite wide interest in CSL, mechanisms responsible for its own regulation are little studied. CSL down-modulation in human dermal fibroblasts (HDFs) leads to conversion into cancer associated fibroblasts (CAF), promoting keratinocyte tumors. We show here that CSL transcript levels differ among HDF strains from different individuals, with negative correlation with genes involved in DNA damage/repair. CSL expression is negatively regulated by stress/DNA damage caused by UVA, Reactive Oxygen Species (ROS), smoke extract, and doxorubicin treatment. P53, a key effector of the DNA damage response, negatively controls CSL gene transcription, through suppression of CSL promoter activity and, indirectly, by increased p21 expression. CSL was previously shown to bind p53 suppressing its activity. The present findings indicate that p53, in turn, decreases CSL expression, which can serve to enhance p53 activity in acute DNA damage response of cells.
DOI: 10.6084/m9.figshare.3364894.v1
title: Negative control of CSL gene transcription by stress/DNA damage response and p53

description: CSL is a key transcriptional repressor and mediator of Notch signaling. Despite wide interest in CSL, mechanisms responsible for its own regulation are little studied. CSL down-modulation in human dermal fibroblasts (HDFs) leads to conversion into cancer associated fibroblasts (CAF), promoting keratinocyte tumors. We show here that CSL transcript levels differ among HDF strains from different individuals, with negative correlation with genes involved in DNA damage/repair. CSL expression is negatively regulated by stress/DNA damage caused by UVA, Reactive Oxygen Species (ROS), smoke extract, and doxorubicin treatment. P53, a key effector of the DNA damage response, negatively controls CSL gene transcription, through suppression of CSL promoter activity and, indirectly, by increased p21 expression. CSL was previously shown to bind p53 suppressing its activity. The present findings indicate that p53, in turn, decreases CSL expression, which can serve to enhance p53 activity in acute DNA damage response of cells.
DOI: 10.6084/m9.figshare.3364891
title: Loss of autophagy enhances MIF/macrophage migration inhibitory factor release by macrophages

description: MIF (macrophage migration inhibitory factor [glycosylation-inhibiting factor]) is a pro-inflammatory cytokine expressed in multiple cells types, including macrophages. MIF plays a pathogenic role in a number of inflammatory diseases and has been linked to tumor progression in some cancers. Previous work has demonstrated that loss of autophagy in macrophages enhances secretion of IL1 family cytokines. Here, we demonstrate that loss of autophagy, by pharmacological inhibition or siRNA silencing of <i>Atg5</i>, enhances MIF secretion by monocytes and macrophages. We further demonstrate that this is dependent on mitochondrial reactive oxygen species (ROS). Induction of autophagy with MTOR inhibitors had no effect on MIF secretion, but amino acid starvation increased secretion. This was unaffected by <i>Atg5</i> siRNA but was again dependent on mitochondrial ROS. Our data demonstrate that autophagic regulation of mitochondrial ROS plays a pivotal role in the regulation of inflammatory cytokine secretion in macrophages, with potential implications for the pathogenesis of inflammatory diseases and cancers.
DOI: 10.6084/m9.figshare.3364891.v1
title: Loss of autophagy enhances MIF/macrophage migration inhibitory factor release by macrophages

description: MIF (macrophage migration inhibitory factor [glycosylation-inhibiting factor]) is a pro-inflammatory cytokine expressed in multiple cells types, including macrophages. MIF plays a pathogenic role in a number of inflammatory diseases and has been linked to tumor progression in some cancers. Previous work has demonstrated that loss of autophagy in macrophages enhances secretion of IL1 family cytokines. Here, we demonstrate that loss of autophagy, by pharmacological inhibition or siRNA silencing of <i>Atg5</i>, enhances MIF secretion by monocytes and macrophages. We further demonstrate that this is dependent on mitochondrial reactive oxygen species (ROS). Induction of autophagy with MTOR inhibitors had no effect on MIF secretion, but amino acid starvation increased secretion. This was unaffected by <i>Atg5</i> siRNA but was again dependent on mitochondrial ROS. Our data demonstrate that autophagic regulation of mitochondrial ROS plays a pivotal role in the regulation of inflammatory cytokine secretion in macrophages, with potential implications for the pathogenesis of inflammatory diseases and cancers.
DOI: 10.6084/m9.figshare.3364840
title: Kite-based Structure-from-Motion survey of southern Topsail Beach, North Carolina, USA, 4/14/2016

description: Digital Surface Model (DSM), Orthophoto, Ground Control Point (GCP) coordinates (recorded using an RTK GNSS system), Structure-from-Motion report (with relevant parameters and spatial accuracy) and raw aerial images from a kite-based survey of South Topsail Beach, NC on April 14th, 2016. DSM and Orthophoto were constructed with 29 GCPs. GCP coordinates are given in NC State Plane Coordinate system, NAD 83, Geoid 09.<br>
DOI: 10.6084/m9.figshare.3364840.v2
title: Kite-based Structure-from-Motion survey of southern Topsail Beach, North Carolina, USA, 4/14/2016

description: Digital Surface Model (DSM), Orthophoto, Ground Control Point (GCP) coordinates (recorded using an RTK GNSS system), Structure-from-Motion report (with relevant parameters and spatial accuracy) and raw aerial images from a kite-based survey of South Topsail Beach, NC on April 14th, 2016. DSM and Orthophoto were constructed with 29 GCPs. GCP coordinates are given in NC State Plane Coordinate system, NAD 83, Geoid 09.<br>