cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1342823.v3
title: TopoSWAT Source

description: Topography exerts critical control on many hydrologic, geomorphologic, and environmental biophysical processes. In order to properly model such dynamics in the Soil and Water Assessment Tool (SWAT), we explicitly integrate topography into the initialization procedure with a purpose-built extension. This ArcMap® toolbox (TopoSWAT) interfaces directly with ArcSWAT, to create multiple SWAT data layers, update the SWAT databases and generate the lookup tables required by the model. User defined data layers are processed in a single-step toolbox and include, aspect, elevation, and topographic index (TI), which are then intersected with the vector FAO Global Soils dataset. The toolbox then builds a soil raster layer at the resolution of the project’s base Digital Elevation Model and creates the ArcSWAT required ‘usersoil’ database table along with the corresponding soil lookup table required to map the specific raster soil values to the soil parameters in the ‘usersoil’ database table. This toolbox effectively creates a new soil dataset that incorporates topographic features. This standardized method and toolset allows SWAT modelers to easily incorporate topographic features they believe are important for their catchments without requiring any changes to the current ArcSWAT initialization system. Some of the topographic features may be necessary for process-based routines that one may want to incorporate into SWAT, e.g., energy-budget snowmelt modeling. However, such routines will need to be added to the SWAT model source code. This SWAT toolbox adds flexibility to SWAT modeling with little extra effort on the part of modelers.
DOI: 10.6084/m9.figshare.1342798.v3
title: Bootstrapped evidence toolbox

description: Bootstrapped evidence toolbox for using the methods described in my article "Non-dichotomous inference using bootstrapped evidence" (currently unpublished)
DOI: 10.6084/m9.figshare.1342795.v1
title: Evolution of the perlecan/HSPG2 gene and its activation in regenerating Nematostella vectensis

description: In situ images, sequence data and phylogeny from our paper concerning the evolution of the perlecan/HSPG2 gene and its activation during regeneration of Nematostella vectensis.
DOI: 10.6084/m9.figshare.1344765.v13
title: SamSrf toolbox for pRF mapping

description: Current version: 5.64 (08-04-2016)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 (12 should also be okay) and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1342796.v2
title: Discordance in Recovery Between Altered Locomotion and Muscle Atrophy Induced by Simulated Microgravity in Rats

description: ABSTRACTExposure to a microgravity environment leads to adverse effects in motion and musculoskeletal properties. However, few studies have investigated the recovery of altered locomotion and muscle atrophy simultaneously. The authors investigated altered locomotion in rats submitted to simulated microgravity by hindlimb unloading for 2 weeks. Motion deficits were characterized by hyperextension of the knees and ankle joints and forward-shifted limb motion. Furthermore, these locomotor deficits did not revert to their original form after a 2-week recovery period, although muscle atrophy in the hindlimbs had recovered, implying discordance in recovery between altered locomotion and muscle atrophy, and that other factors such as neural drives might control behavioral adaptations to microgravity.
DOI: 10.6084/m9.figshare.1342798.v2
title: Bootstrapped evidence toolbox

description: Bootstrapped evidence toolbox for using the methods described in my article "Non-dichotomous inference using bootstrapped evidence" (currently unpublished)
DOI: 10.6084/m9.figshare.1342796.v1
title: Discordance in Recovery Between Altered Locomotion and Muscle Atrophy Induced by Simulated Microgravity in Rats

description: ABSTRACT.Exposure to a microgravity environment leads to adverse effects in motion and musculoskeletal properties. However, few studies have investigated the recovery of altered locomotion and muscle atrophy simultaneously. The authors investigated altered locomotion in rats submitted to simulated microgravity by hindlimb unloading for 2 weeks. Motion deficits were characterized by hyperextension of the knees and ankle joints and forward-shifted limb motion. Furthermore, these locomotor deficits did not revert to their original form after a 2-week recovery period, although muscle atrophy in the hindlimbs had recovered, implying discordance in recovery between altered locomotion and muscle atrophy, and that other factors such as neural drives might control behavioral adaptations to microgravity.
DOI: 10.6084/m9.figshare.1344765.v14
title: SamSrf toolbox for pRF mapping

description: Current version: 5.65 (30-06-2016)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 (12 should also be okay) and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1344765.v15
title: SamSrf toolbox for pRF mapping

description: Current version: 5.66 (05-08-2016)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 (12 should also be okay) and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1342789.v1
title: Stranglehold on the Spindle Assembly Checkpoint: The Human Papillomavirus E2 Protein Provokes BUBR1-dependent Aneuploidy

description: ABSTRACTThe Human Papillomavirus (HPV) E2 protein, which inhibits the E6 and E7 viral oncogenes, is believed to have anti-oncogenic properties. Here, we challenge this view and show that HPV-18 E2 over-activates the Spindle Assembly Checkpoint (SAC) and induces DNA breaks in mitosis followed by aneuploidy. This phenotype is associated with interaction of E2 with the Mitotic Checkpoint Complex (MCC) proteins Cdc20, MAD2 and BUBR1. While BUBR1 silencing rescues the mitotic phenotype induced by E2, p53 silencing or presence of E6/E7 (inactivating p53 and increasing BUBR1 levels respectively) both amplify it. This work pinpoints E2 as a key protein in the initiation of HPV-induced cervical cancer and identifies the SAC as a target for oncogenic pathogens. Moreover, our results suggest a role of p53 in regulating the mitotic process itself and highlight SAC over-activation in a p53-negative context as a highly pathogenic event.
DOI: 10.6084/m9.figshare.1344765.v16
title: SamSrf toolbox for pRF mapping

description: Current version: 5.67 (15-08-2016)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 (12 should also be okay) and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1344765.v17
title: SamSrf toolbox for pRF mapping

description: Current version: 5.68 (08-09-2016)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 (12 should also be okay) and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1342789
title: Stranglehold on the spindle assembly checkpoint: the human papillomavirus E2 protein provokes BUBR1-dependent aneuploidy

description: The Human Papillomavirus (HPV) E2 protein, which inhibits the E6 and E7 viral oncogenes, is believed to have anti-oncogenic properties. Here, we challenge this view and show that HPV-18 E2 over-activates the Spindle Assembly Checkpoint (SAC) and induces DNA breaks in mitosis followed by aneuploidy. This phenotype is associated with interaction of E2 with the Mitotic Checkpoint Complex (MCC) proteins Cdc20, MAD2 and BUBR1. While BUBR1 silencing rescues the mitotic phenotype induced by E2, p53 silencing or presence of E6/E7 (inactivating p53 and increasing BUBR1 levels respectively) both amplify it. This work pinpoints E2 as a key protein in the initiation of HPV-induced cervical cancer and identifies the SAC as a target for oncogenic pathogens. Moreover, our results suggest a role of p53 in regulating the mitotic process itself and highlight SAC over-activation in a p53-negative context as a highly pathogenic event.
DOI: 10.6084/m9.figshare.1342789.v2
title: Stranglehold on the spindle assembly checkpoint: the human papillomavirus E2 protein provokes BUBR1-dependent aneuploidy

description: The Human Papillomavirus (HPV) E2 protein, which inhibits the E6 and E7 viral oncogenes, is believed to have anti-oncogenic properties. Here, we challenge this view and show that HPV-18 E2 over-activates the Spindle Assembly Checkpoint (SAC) and induces DNA breaks in mitosis followed by aneuploidy. This phenotype is associated with interaction of E2 with the Mitotic Checkpoint Complex (MCC) proteins Cdc20, MAD2 and BUBR1. While BUBR1 silencing rescues the mitotic phenotype induced by E2, p53 silencing or presence of E6/E7 (inactivating p53 and increasing BUBR1 levels respectively) both amplify it. This work pinpoints E2 as a key protein in the initiation of HPV-induced cervical cancer and identifies the SAC as a target for oncogenic pathogens. Moreover, our results suggest a role of p53 in regulating the mitotic process itself and highlight SAC over-activation in a p53-negative context as a highly pathogenic event.
DOI: 10.6084/m9.figshare.1342789.v4
title: Stranglehold on the spindle assembly checkpoint: the human papillomavirus E2 protein provokes BUBR1-dependent aneuploidy

description: The Human Papillomavirus (HPV) E2 protein, which inhibits the E6 and E7 viral oncogenes, is believed to have anti-oncogenic properties. Here, we challenge this view and show that HPV-18 E2 over-activates the Spindle Assembly Checkpoint (SAC) and induces DNA breaks in mitosis followed by aneuploidy. This phenotype is associated with interaction of E2 with the Mitotic Checkpoint Complex (MCC) proteins Cdc20, MAD2 and BUBR1. While BUBR1 silencing rescues the mitotic phenotype induced by E2, p53 silencing or presence of E6/E7 (inactivating p53 and increasing BUBR1 levels respectively) both amplify it. This work pinpoints E2 as a key protein in the initiation of HPV-induced cervical cancer and identifies the SAC as a target for oncogenic pathogens. Moreover, our results suggest a role of p53 in regulating the mitotic process itself and highlight SAC over-activation in a p53-negative context as a highly pathogenic event.
DOI: 10.6084/m9.figshare.1342789.v3
title: Stranglehold on the spindle assembly checkpoint: the human papillomavirus E2 protein provokes BUBR1-dependent aneuploidy

description: The Human Papillomavirus (HPV) E2 protein, which inhibits the E6 and E7 viral oncogenes, is believed to have anti-oncogenic properties. Here, we challenge this view and show that HPV-18 E2 over-activates the Spindle Assembly Checkpoint (SAC) and induces DNA breaks in mitosis followed by aneuploidy. This phenotype is associated with interaction of E2 with the Mitotic Checkpoint Complex (MCC) proteins Cdc20, MAD2 and BUBR1. While BUBR1 silencing rescues the mitotic phenotype induced by E2, p53 silencing or presence of E6/E7 (inactivating p53 and increasing BUBR1 levels respectively) both amplify it. This work pinpoints E2 as a key protein in the initiation of HPV-induced cervical cancer and identifies the SAC as a target for oncogenic pathogens. Moreover, our results suggest a role of p53 in regulating the mitotic process itself and highlight SAC over-activation in a p53-negative context as a highly pathogenic event.
DOI: 10.6084/m9.figshare.1344765.v18
title: SamSrf toolbox for pRF mapping

description: Current version: 5.69 (08-12-2016)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 (12 should also be okay) and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1344765.v20
title: SamSrf toolbox for pRF mapping

description: Current version: 5.8 (13-04-2017)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 or SPM12 and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1344765.v21
title: SamSrf toolbox for pRF mapping

description: Current version: 5.81 (05-05-2017)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 or SPM12 and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1342777.v1
title: Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice

description: The Suv39h1 and Suv39h2 H3K9 histone methyltransferases (HMTs) have a conserved role in the formation of constitutive heterochromatin and gene silencing. Using a transgenic mouse model system we demonstrate that elevated expression of Suv39h1 increases global H3K9me3 levels <i>in vivo</i>. More specifically, Suv39h1 overexpression enhances the imposition of H3K9me3 levels at constitutive heterochromatin at telomeric and major satellite repeats in primary mouse embryonic fibroblasts. Chromatin compaction is paralleled by telomere shortening, indicating that telomere length is controlled by H3K9me3 density at telomeres. We further show that increased Suv39h1 levels result in an impaired clonogenic potential of transgenic epidermal stem cells and Ras/E1A transduced transgenic primary mouse embryonic fibroblasts. Importantly, Suv39h1 overexpression in mice confers resistance to a DMBA/TPA induced skin carcinogenesis protocol that is characterized by the accumulation of activating H-<i>ras</i> mutations. Our results provide genetic evidence that Suv39h1 controls telomere homeostasis and mediates resistance to oncogenic stress <i>in vivo</i>. This identifies Suv39h1 as an interesting target to improve oncogene induced senescence in premalignant lesions.
DOI: 10.6084/m9.figshare.1344765.v22
title: SamSrf toolbox for pRF mapping

description: Current version: 5.82 (08-05-2017)Our Matlab toolbox for pRF mapping analysis. Uses SPM8 or SPM12 and FreeSurfer functionality for preprocessing. Also requires Statistics Toolbox, Optimization Toolbox, and Curve Fitting Toolbox (not strictly necessary) for Matlab.<br><br>An extensive documentation "cookbook" is included. Please contact Sam (sampendu.wordpress.com) for any questions but please be advised that we are not able to provide tech support for people we don't collaborate with.As of version 5.63, we included a new tutorial explaining how to delineate visual areas using the DelineationTool in MatLab and giving advice on what to do with tricky retinotopic maps.<br>
DOI: 10.6084/m9.figshare.1342777.v2
title: Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice

description: The Suv39h1 and Suv39h2 H3K9 histone methyltransferases (HMTs) have a conserved role in the formation of constitutive heterochromatin and gene silencing. Using a transgenic mouse model system we demonstrate that elevated expression of Suv39h1 increases global H3K9me3 levels <i>in vivo</i>. More specifically, Suv39h1 overexpression enhances the imposition of H3K9me3 levels at constitutive heterochromatin at telomeric and major satellite repeats in primary mouse embryonic fibroblasts. Chromatin compaction is paralleled by telomere shortening, indicating that telomere length is controlled by H3K9me3 density at telomeres. We further show that increased Suv39h1 levels result in an impaired clonogenic potential of transgenic epidermal stem cells and Ras/E1A transduced transgenic primary mouse embryonic fibroblasts. Importantly, Suv39h1 overexpression in mice confers resistance to a DMBA/TPA induced skin carcinogenesis protocol that is characterized by the accumulation of activating H-<i>ras</i> mutations. Our results provide genetic evidence that Suv39h1 controls telomere homeostasis and mediates resistance to oncogenic stress <i>in vivo</i>. This identifies Suv39h1 as an interesting target to improve oncogene induced senescence in premalignant lesions.
DOI: 10.6084/m9.figshare.1342777
title: Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice

description: The Suv39h1 and Suv39h2 H3K9 histone methyltransferases (HMTs) have a conserved role in the formation of constitutive heterochromatin and gene silencing. Using a transgenic mouse model system we demonstrate that elevated expression of Suv39h1 increases global H3K9me3 levels <i>in vivo</i>. More specifically, Suv39h1 overexpression enhances the imposition of H3K9me3 levels at constitutive heterochromatin at telomeric and major satellite repeats in primary mouse embryonic fibroblasts. Chromatin compaction is paralleled by telomere shortening, indicating that telomere length is controlled by H3K9me3 density at telomeres. We further show that increased Suv39h1 levels result in an impaired clonogenic potential of transgenic epidermal stem cells and Ras/E1A transduced transgenic primary mouse embryonic fibroblasts. Importantly, Suv39h1 overexpression in mice confers resistance to a DMBA/TPA induced skin carcinogenesis protocol that is characterized by the accumulation of activating H-<i>ras</i> mutations. Our results provide genetic evidence that Suv39h1 controls telomere homeostasis and mediates resistance to oncogenic stress <i>in vivo</i>. This identifies Suv39h1 as an interesting target to improve oncogene induced senescence in premalignant lesions.
DOI: 10.6084/m9.figshare.1342777.v3
title: Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice

description: The Suv39h1 and Suv39h2 H3K9 histone methyltransferases (HMTs) have a conserved role in the formation of constitutive heterochromatin and gene silencing. Using a transgenic mouse model system we demonstrate that elevated expression of Suv39h1 increases global H3K9me3 levels <i>in vivo</i>. More specifically, Suv39h1 overexpression enhances the imposition of H3K9me3 levels at constitutive heterochromatin at telomeric and major satellite repeats in primary mouse embryonic fibroblasts. Chromatin compaction is paralleled by telomere shortening, indicating that telomere length is controlled by H3K9me3 density at telomeres. We further show that increased Suv39h1 levels result in an impaired clonogenic potential of transgenic epidermal stem cells and Ras/E1A transduced transgenic primary mouse embryonic fibroblasts. Importantly, Suv39h1 overexpression in mice confers resistance to a DMBA/TPA induced skin carcinogenesis protocol that is characterized by the accumulation of activating H-<i>ras</i> mutations. Our results provide genetic evidence that Suv39h1 controls telomere homeostasis and mediates resistance to oncogenic stress <i>in vivo</i>. This identifies Suv39h1 as an interesting target to improve oncogene induced senescence in premalignant lesions.
DOI: 10.6084/m9.figshare.1342777.v4
title: Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice

description: The Suv39h1 and Suv39h2 H3K9 histone methyltransferases (HMTs) have a conserved role in the formation of constitutive heterochromatin and gene silencing. Using a transgenic mouse model system we demonstrate that elevated expression of Suv39h1 increases global H3K9me3 levels <i>in vivo</i>. More specifically, Suv39h1 overexpression enhances the imposition of H3K9me3 levels at constitutive heterochromatin at telomeric and major satellite repeats in primary mouse embryonic fibroblasts. Chromatin compaction is paralleled by telomere shortening, indicating that telomere length is controlled by H3K9me3 density at telomeres. We further show that increased Suv39h1 levels result in an impaired clonogenic potential of transgenic epidermal stem cells and Ras/E1A transduced transgenic primary mouse embryonic fibroblasts. Importantly, Suv39h1 overexpression in mice confers resistance to a DMBA/TPA induced skin carcinogenesis protocol that is characterized by the accumulation of activating H-<i>ras</i> mutations. Our results provide genetic evidence that Suv39h1 controls telomere homeostasis and mediates resistance to oncogenic stress <i>in vivo</i>. This identifies Suv39h1 as an interesting target to improve oncogene induced senescence in premalignant lesions.