cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3205285.v1
title: No light at the end of the tunnel: Shading impacts on biological communities from subtropical rocky shores

description: Dataset refers to André L. Pardal-Souza's master thesis. Those data were used on writing a manuscript sent to Journal of Applied Ecology.
DOI: 10.6084/m9.figshare.3205249
title: geauxdock.tar.gz

description: <strong>GeauxDock</strong> is an ultra-fast automated docking program, designed to predict how small ligands bind to pharmacologically relevant macromolecules. GeauxDock employs a novel hybrid force field, a mixed-resolution representation of protein-ligand complexes, and a Monte Carlo protocol for the efficient sampling of conformational space.<br><br><br><br>
DOI: 10.6084/m9.figshare.3205249.v1
title: geauxdock.tar.gz

description: <strong>GeauxDock</strong> is an ultra-fast automated docking program, designed to predict how small ligands bind to pharmacologically relevant macromolecules. GeauxDock employs a novel hybrid force field, a mixed-resolution representation of protein-ligand complexes, and a Monte Carlo protocol for the efficient sampling of conformational space.<br><br><br><br>
DOI: 10.6084/m9.figshare.3205273.v2
title: Pruning

description: More info to come
DOI: 10.6084/m9.figshare.3205228
title: Mesenchymal stromal cells having inactivated <i>RB1</i> survive following low irradiation and accumulate damaged DNA: Hints for side effects following radiotherapy

description: Following radiotherapy, bone sarcomas account for a significant percentage of recurring tumors. This risk is further increased in patients with hereditary retinoblastoma that undergo radiotherapy. We analyzed the effect of low and medium dose radiation on mesenchymal stromal cells (MSCs) with inactivated <i>RB1</i> gene to gain insights on the molecular mechanisms that can induce second malignant neoplasm in cancer survivors. MSC cultures contain subpopulations of mesenchymal stem cells and committed progenitors that can differentiate into mesodermal derivatives: adipocytes, chondrocytes, and osteocytes. These stem cells and committed osteoblast precursors are the cell of origin in osteosarcoma, and <i>RB1</i> gene mutations have a strong role in its pathogenesis. Following 40 and 2000 mGy X-ray exposure, MSCs with inactivated <i>RB1</i> do not proliferate and accumulate high levels of unrepaired DNA as detected by persistence of gamma-H2AX foci. In samples with inactivated <i>RB1</i> the radiation treatment did not increase apoptosis, necrosis or senescence versus untreated cells. Following radiation, CFU analysis showed a discrete number of cells with clonogenic capacity in cultures with silenced <i>RB1</i>. We extended our analysis to the other members of retinoblastoma gene family: <i>RB2/P130</i> and <i>P107</i>. Also in the MSCs with silenced <i>RB2/P130</i> and <i>P107</i> we detected the presence of cells with unrepaired DNA following X-ray irradiation. Cells with unrepaired DNA may represent a reservoir of cells that may undergo neoplastic transformation. Our study suggests that, following radiotherapy, cancer patients with mutations of retinoblastoma genes may be under strict controls to evaluate onset of secondary neoplasms following radiotherapy.
DOI: 10.6084/m9.figshare.3205234
title: Identification of miR-34 regulatory networks in settings of disease and antimiR-therapy: Implications for treating cardiac pathology and other diseases

description: Expression of the miR-34 family (miR-34a, -34b, -34c) is elevated in settings of heart disease, and inhibition with antimiR-34a/antimiR-34 has emerged as a promising therapeutic strategy. Under chronic cardiac disease settings, targeting the entire miR-34 family is more effective than targeting miR-34a alone. The identification of transcription factor (TF)-miRNA regulatory networks has added complexity to understanding the therapeutic potential of miRNA-based therapies. Here, we sought to determine whether antimiR-34 targets secondary miRNAs via TFs which could contribute to antimiR-34-mediated protection. Using miRNA-Seq we identified differentially regulated miRNAs in hearts from mice with cardiac pathology due to transverse aortic constriction (TAC), and focused on miRNAs which were also regulated by antimiR-34. Two clusters of stress-responsive miRNAs were classified as “pathological” and “cardioprotective,” respectively. Using ChIPBase we identified 45 TF binding sites on the promoters of “pathological” and “cardioprotective” miRNAs, and 5 represented direct targets of miR-34, with the capacity to regulate other miRNAs. Knockdown studies in a cardiomyoblast cell line demonstrated that expression of 2 “pathological” miRNAs (let-7e, miR-31) was regulated by one of the identified TFs. Furthermore, by qPCR we confirmed that expression of let-7e and miR-31 was lower in hearts from antimiR-34 treated TAC mice; this may explain why targeting the entire miR-34 family is more effective than targeting miR-34a alone. Finally, we showed that Acsl4 (a common target of miR-34, let-7e and miR-31) was increased in hearts from TAC antimiR-34 treated mice. In summary, antimiR-34 regulates the expression of other miRNAs and this has implications for drug development.
DOI: 10.6084/m9.figshare.3205237
title: Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction

description: Renal fibrosis is the final, common pathway of end-stage renal disease. Whether and how autophagy contributes to renal fibrosis remains unclear. Here we first detected persistent autophagy in kidney proximal tubules in the renal fibrosis model of unilateral ureteral obstruction (UUO) in mice. UUO-associated fibrosis was suppressed by pharmacological inhibitors of autophagy and also by kidney proximal tubule-specific knockout of autophagy-related 7 (PT-<i>Atg7</i> KO). Consistently, proliferation and activation of fibroblasts, as indicated by the expression of ACTA2/α-smooth muscle actin and VIM (vimentin), was inhibited in PT-<i>Atg7</i> KO mice, so was the accumulation of extracellular matrix components including FN1 (fibronectin 1) and collagen fibrils. Tubular atrophy, apoptosis, nephron loss, and interstitial macrophage infiltration were all inhibited in these mice. Moreover, these mice showed a specific suppression of the expression of a profibrotic factor FGF2 (fibroblast growth factor 2). In vitro, TGFB1 (transforming growth factor β 1) induced autophagy, apoptosis, and FN1 accumulation in primary proximal tubular cells. Inhibition of autophagy suppressed FN1 accumulation and apoptosis, while enhancement of autophagy increased TGFB1-induced-cell death. These results suggest that persistent activation of autophagy in kidney proximal tubules promotes renal interstitial fibrosis during UUO. The profibrotic function of autophagy is related to the regulation on tubular cell death, interstitial inflammation, and the production of profibrotic factors.
DOI: 10.6084/m9.figshare.3205234.v1
title: Identification of miR-34 regulatory networks in settings of disease and antimiR-therapy: Implications for treating cardiac pathology and other diseases

description: Expression of the miR-34 family (miR-34a, -34b, -34c) is elevated in settings of heart disease, and inhibition with antimiR-34a/antimiR-34 has emerged as a promising therapeutic strategy. Under chronic cardiac disease settings, targeting the entire miR-34 family is more effective than targeting miR-34a alone. The identification of transcription factor (TF)-miRNA regulatory networks has added complexity to understanding the therapeutic potential of miRNA-based therapies. Here, we sought to determine whether antimiR-34 targets secondary miRNAs via TFs which could contribute to antimiR-34-mediated protection. Using miRNA-Seq we identified differentially regulated miRNAs in hearts from mice with cardiac pathology due to transverse aortic constriction (TAC), and focused on miRNAs which were also regulated by antimiR-34. Two clusters of stress-responsive miRNAs were classified as “pathological” and “cardioprotective,” respectively. Using ChIPBase we identified 45 TF binding sites on the promoters of “pathological” and “cardioprotective” miRNAs, and 5 represented direct targets of miR-34, with the capacity to regulate other miRNAs. Knockdown studies in a cardiomyoblast cell line demonstrated that expression of 2 “pathological” miRNAs (let-7e, miR-31) was regulated by one of the identified TFs. Furthermore, by qPCR we confirmed that expression of let-7e and miR-31 was lower in hearts from antimiR-34 treated TAC mice; this may explain why targeting the entire miR-34 family is more effective than targeting miR-34a alone. Finally, we showed that Acsl4 (a common target of miR-34, let-7e and miR-31) was increased in hearts from TAC antimiR-34 treated mice. In summary, antimiR-34 regulates the expression of other miRNAs and this has implications for drug development.
DOI: 10.6084/m9.figshare.3205237.v1
title: Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction

description: Renal fibrosis is the final, common pathway of end-stage renal disease. Whether and how autophagy contributes to renal fibrosis remains unclear. Here we first detected persistent autophagy in kidney proximal tubules in the renal fibrosis model of unilateral ureteral obstruction (UUO) in mice. UUO-associated fibrosis was suppressed by pharmacological inhibitors of autophagy and also by kidney proximal tubule-specific knockout of autophagy-related 7 (PT-<i>Atg7</i> KO). Consistently, proliferation and activation of fibroblasts, as indicated by the expression of ACTA2/α-smooth muscle actin and VIM (vimentin), was inhibited in PT-<i>Atg7</i> KO mice, so was the accumulation of extracellular matrix components including FN1 (fibronectin 1) and collagen fibrils. Tubular atrophy, apoptosis, nephron loss, and interstitial macrophage infiltration were all inhibited in these mice. Moreover, these mice showed a specific suppression of the expression of a profibrotic factor FGF2 (fibroblast growth factor 2). In vitro, TGFB1 (transforming growth factor β 1) induced autophagy, apoptosis, and FN1 accumulation in primary proximal tubular cells. Inhibition of autophagy suppressed FN1 accumulation and apoptosis, while enhancement of autophagy increased TGFB1-induced-cell death. These results suggest that persistent activation of autophagy in kidney proximal tubules promotes renal interstitial fibrosis during UUO. The profibrotic function of autophagy is related to the regulation on tubular cell death, interstitial inflammation, and the production of profibrotic factors.
DOI: 10.6084/m9.figshare.3205219
title: Prosurvival AMBRA1 turns into a proapoptotic BH3-like protein during mitochondrial apoptosis

description: Autophagy and apoptosis are 2 stress-response mechanisms that are closely interconnected. However, the molecular interplays between these 2 pathways remain to be clarified. Here we report that the crucial proautophagic factor AMBRA1 can act as a positive mediator of mitochondrial apoptosis. Indeed, we show that, in a proapoptotic positive feedback loop, the C-terminal part of AMBRA1, generated by CASP/CASPASE cleavage upon apoptosis induction, inhibits the antiapoptotic factor BCL2 by a direct binding through its BH3-like domain. The mitochondrial AMBRA1-BCL2 complex is thus at the crossroad between autophagy and cell death and may represent a novel target in development of therapeutic approaches in clinical diseases.
DOI: 10.6084/m9.figshare.3205219.v1
title: Prosurvival AMBRA1 turns into a proapoptotic BH3-like protein during mitochondrial apoptosis

description: Autophagy and apoptosis are 2 stress-response mechanisms that are closely interconnected. However, the molecular interplays between these 2 pathways remain to be clarified. Here we report that the crucial proautophagic factor AMBRA1 can act as a positive mediator of mitochondrial apoptosis. Indeed, we show that, in a proapoptotic positive feedback loop, the C-terminal part of AMBRA1, generated by CASP/CASPASE cleavage upon apoptosis induction, inhibits the antiapoptotic factor BCL2 by a direct binding through its BH3-like domain. The mitochondrial AMBRA1-BCL2 complex is thus at the crossroad between autophagy and cell death and may represent a novel target in development of therapeutic approaches in clinical diseases.
DOI: 10.6084/m9.figshare.3205210
title: Patient-Centered Communication for Discussing Oncotype DX Testing

description: Oncotype DX testing (ODX), a tumor gene expression test, may improve breast cancer care, however, communicating results remains challenging. We identified patient-centered communication strategies/gaps for discussing ODX results. We applied a patient-centered communication framework to analyze qualitative interviews with oncologists about how they communicate about ODX with patients, using template analysis in Atlas.ti. Overall, providers discussed four patient-centered communication domains: exchanging information, assessing uncertainty, making decisions and cross-cutting themes. Providers did not report discussing emotional aspects of managing uncertainty, assessing decision-making preferences, and evaluating decisions. A patient-centered approach may be a model for communicating about tumor gene expression tests.
DOI: 10.6084/m9.figshare.3205210.v1
title: Patient-Centered Communication for Discussing Oncotype DX Testing

description: Oncotype DX testing (ODX), a tumor gene expression test, may improve breast cancer care, however, communicating results remains challenging. We identified patient-centered communication strategies/gaps for discussing ODX results. We applied a patient-centered communication framework to analyze qualitative interviews with oncologists about how they communicate about ODX with patients, using template analysis in Atlas.ti. Overall, providers discussed four patient-centered communication domains: exchanging information, assessing uncertainty, making decisions and cross-cutting themes. Providers did not report discussing emotional aspects of managing uncertainty, assessing decision-making preferences, and evaluating decisions. A patient-centered approach may be a model for communicating about tumor gene expression tests.
DOI: 10.6084/m9.figshare.3205216
title: Hybrid mechanosensing system to generate the polarity needed for migration in fish keratocytes

description: Crawling cells can generate polarity for migration in response to forces applied from the substratum. Such reaction varies according to cell type: there are both fast- and slow-crawling cells. In response to periodic stretching of the elastic substratum, the intracellular stress fibers in slow-crawling cells, such as fibroblasts, rearrange themselves perpendicular to the direction of stretching, with the result that the shape of the cells extends in that direction; whereas fast-crawling cells, such as neutrophil-like differentiated HL-60 cells and <i>Dictyostelium</i> cells, which have no stress fibers, migrate perpendicular to the stretching direction. Fish epidermal keratocytes are another type of fast-crawling cell. However, they have stress fibers in the cell body, which gives them a typical slow-crawling cell structure. In response to periodic stretching of the elastic substratum, intact keratocytes rearrange their stress fibers perpendicular to the direction of stretching in the same way as fibroblasts and migrate parallel to the stretching direction, while blebbistatin-treated stress fiber-less keratocytes migrate perpendicular to the stretching direction, in the same way as seen in HL-60 cells and <i>Dictyostelium</i> cells. Our results indicate that keratocytes have a hybrid mechanosensing system that comprises elements of both fast- and slow-crawling cells, to generate the polarity needed for migration.
DOI: 10.6084/m9.figshare.3205216.v1
title: Hybrid mechanosensing system to generate the polarity needed for migration in fish keratocytes

description: Crawling cells can generate polarity for migration in response to forces applied from the substratum. Such reaction varies according to cell type: there are both fast- and slow-crawling cells. In response to periodic stretching of the elastic substratum, the intracellular stress fibers in slow-crawling cells, such as fibroblasts, rearrange themselves perpendicular to the direction of stretching, with the result that the shape of the cells extends in that direction; whereas fast-crawling cells, such as neutrophil-like differentiated HL-60 cells and <i>Dictyostelium</i> cells, which have no stress fibers, migrate perpendicular to the stretching direction. Fish epidermal keratocytes are another type of fast-crawling cell. However, they have stress fibers in the cell body, which gives them a typical slow-crawling cell structure. In response to periodic stretching of the elastic substratum, intact keratocytes rearrange their stress fibers perpendicular to the direction of stretching in the same way as fibroblasts and migrate parallel to the stretching direction, while blebbistatin-treated stress fiber-less keratocytes migrate perpendicular to the stretching direction, in the same way as seen in HL-60 cells and <i>Dictyostelium</i> cells. Our results indicate that keratocytes have a hybrid mechanosensing system that comprises elements of both fast- and slow-crawling cells, to generate the polarity needed for migration.
DOI: 10.6084/m9.figshare.3205228.v1
title: Mesenchymal stromal cells having inactivated <i><b>RB1</b></i> survive following low irradiation and accumulate damaged DNA: hints for side effects following radiotherapy

description: Following radiotherapy, bone sarcomas account for a significant percentage of recurring tumors. This risk is further increased in patients with hereditary retinoblastoma that undergo radiotherapy. We analyzed the effect of low and medium dose radiation on mesenchymal stromal cells (MSCs) with inactivated <i>RB1</i> gene to gain insights on the molecular mechanisms that can induce second malignant neoplasm in cancer survivors. MSC cultures contain subpopulations of mesenchymal stem cells and committed progenitors that can differentiate into mesodermal derivatives: adipocytes, chondrocytes, and osteocytes. These stem cells and committed osteoblast precursors are the cell of origin in osteosarcoma, and <i>RB1</i> gene mutations have a strong role in its pathogenesis. Following 40 and 2000 mGy X-ray exposure, MSCs with inactivated <i>RB1</i> do not proliferate and accumulate high levels of unrepaired DNA as detected by persistence of gamma-H2AX foci. In samples with inactivated <i>RB1</i> the radiation treatment did not increase apoptosis, necrosis or senescence versus untreated cells. Following radiation, CFU analysis showed a discrete number of cells with clonogenic capacity in cultures with silenced <i>RB1</i>. We extended our analysis to the other members of retinoblastoma gene family: <i>RB2/P130</i> and <i>P107</i>. Also in the MSCs with silenced <i>RB2/P130</i> and <i>P107</i> we detected the presence of cells with unrepaired DNA following X-ray irradiation. Cells with unrepaired DNA may represent a reservoir of cells that may undergo neoplastic transformation. Our study suggests that, following radiotherapy, cancer patients with mutations of retinoblastoma genes may be under strict controls to evaluate onset of secondary neoplasms following radiotherapy.
DOI: 10.6084/m9.figshare.3205018
title: Open Data Analytics Reference Model (ODARM)

description: This poster presents an Open Data Analytics Reference Model for teaching and designing highly scalable distributed analytic systems.
DOI: 10.6084/m9.figshare.3205075
title: NEON Data Institute 2016 - Remote Sensing Data Subsets - Domain 17 - California Field Sites

description: Teaching data subsets for the NEON Lower Teakettle (TEAK), San Joaquin Experimental Range (SJER), and Soaproot Saddle (SOAP) field sites in California (Domain 17). These data sets are used with the NEON Data Institute 2016.<br>This teaching data subset is used for several tutorials on the NEON website (neonscience.org). The dataset is for educational purposes, data for research purposes can be obtained from the NEON Data Portal (data.neonscience.org).<br>
DOI: 10.6084/m9.figshare.3205018.v1
title: Open Data Analytics Reference Model (ODARM)

description: This poster presents an Open Data Analytics Reference Model for teaching and designing highly scalable distributed analytic systems.
DOI: 10.6084/m9.figshare.3204931
title: Fossil evidence of social insect commensalism in the Phoridae (Insecta: Diptera)

description: Fossil phorid flies display various levels of morphological change that are correlated with myrmecophily (association with ants) and termitophily (association with termites) in the modern fauna. Three discrete episodes in the evolution of limuloidy, a defensive body form, are documented from Eocene Baltic amber. Extinct fossil stem-group taxa of the modern myrmecophilous genus <i>Aenigmatias</i> Meinert are described, with three new species – <i>A. longicornis</i> sp. nov., <i>A. primitivus</i> sp. nov. and <i>A. nigeroticus</i> sp. nov. – recognized and illustrated. <i>Protoplatyphora</i> Brues is synonymized with <i>Aenigmatias</i>, with its single previously described species, <i>A. tertiarius</i> (Brues), considered a new combination. <i>Chaetopleurophora bisetosa</i> Brown, 2007 is transferred to <i>Aenigmatias</i> as <i>A. bisetosus</i> (comb. nov.). An unrelated <i>Aenigmatias</i>-like fossil is described as <i>Pseudaenigmatias ctenitibia</i> gen. et sp. nov., and belongs to a modern termitophilous clade. <i>Limulomyia tyche</i> Brown, 1999 is interpreted as a separate, already highly limuloid lineage not related to either of the other two limuloid groups. A key to fossil <i>Aenigmatias</i> is given, along with a phylogenetic analysis of fossil taxa. Fossil specimens have profound implications for our knowledge of the evolution of the limuloid body form found in modern species of <i>Aenigmatias</i>. http://zoobank.org/urn:lsid:zoobank.org:pub:DE779D49-7636-4B1D-9F7D-CF3FF6D3CE97
DOI: 10.6084/m9.figshare.3205075.v1
title: Teakettle Remote Sensing Data Subset

description: A test subset for the NEON Teakettle Field Site in Southern California (D17)
DOI: 10.6084/m9.figshare.3204931.v1
title: Fossil evidence of social insect commensalism in the Phoridae (Insecta: Diptera)

description: Fossil phorid flies display various levels of morphological change that are correlated with myrmecophily (association with ants) and termitophily (association with termites) in the modern fauna. Three discrete episodes in the evolution of limuloidy, a defensive body form, are documented from Eocene Baltic amber. Extinct fossil stem-group taxa of the modern myrmecophilous genus <i>Aenigmatias</i> Meinert are described, with three new species – <i>A. longicornis</i> sp. nov., <i>A. primitivus</i> sp. nov. and <i>A. nigeroticus</i> sp. nov. – recognized and illustrated. <i>Protoplatyphora</i> Brues is synonymized with <i>Aenigmatias</i>, with its single previously described species, <i>A. tertiarius</i> (Brues), considered a new combination. <i>Chaetopleurophora bisetosa</i> Brown, 2007 is transferred to <i>Aenigmatias</i> as <i>A. bisetosus</i> (comb. nov.). An unrelated <i>Aenigmatias</i>-like fossil is described as <i>Pseudaenigmatias ctenitibia</i> gen. et sp. nov., and belongs to a modern termitophilous clade. <i>Limulomyia tyche</i> Brown, 1999 is interpreted as a separate, already highly limuloid lineage not related to either of the other two limuloid groups. A key to fossil <i>Aenigmatias</i> is given, along with a phylogenetic analysis of fossil taxa. Fossil specimens have profound implications for our knowledge of the evolution of the limuloid body form found in modern species of <i>Aenigmatias</i>. http://zoobank.org/urn:lsid:zoobank.org:pub:DE779D49-7636-4B1D-9F7D-CF3FF6D3CE97
DOI: 10.6084/m9.figshare.3205075.v2
title: Teakettle Remote Sensing Data Subset

description: A test subset for the NEON Teakettle Field Site in Southern California (D17)