cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.13003190.v1
title: Set 1_S2_molecule_chkpt

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003196
title: Set 1_S2_filtered_gene

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.5281/zenodo.4048817
title: Lung MRI Raw Data Acquired with 3D UTE Radial Trajectory

description: This repository contains the raw data for the second lung MRI result in Extreme MRI: Large-Scale Volumetric Dynamic Imaging from Continuous Non-Gated Acquisitions. The data is stored as numpy arrays, containing k-space data (ksp.npy), coordinates (coord.npy), and density compensation factors (dcf.npy). Code to process and reconstruct the data is available here: https://github.com/mikgroup/extreme_mri For more information about how the data is acquired, please see the linked paper.
DOI: 10.5281/zenodo.3672169
title: Lung MRI Raw Data Acquired with 3D UTE Radial Trajectory

description: This repository contains the raw data for the second lung MRI result in Extreme MRI: Large-Scale Volumetric Dynamic Imaging from Continuous Non-Gated Acquisitions. The data is stored as numpy arrays, containing k-space data (ksp.npy), coordinates (coord.npy), and density compensation factors (dcf.npy). Code to process and reconstruct the data is available here: https://github.com/mikgroup/extreme_mri For more information about how the data is acquired, please see the linked paper.
DOI: 10.5281/zenodo.4048310
title: Monthly CO2 emissions projections from 2015-2025: modified SSP2-4.5 to account for COVID-19 impacts on sector activity

description: Monthly CO2 emissions projections 2015-2025, modified by country-specific impacts of COVID-19 lockdown in 2020-2023, with 4 different projections for the period 2024-2025. This repository holds the netcdf files for CO2 emissions from ground-level and aviation sources from the MESSAGE_GLOBIOM scenario SSP2-4.5, from the Scenario4MIPs database (https://esgf-node.llnl.gov/search/input4mips/), modified by the country and sector activity levels associated with lockdown for 2020. Sector activity level in 2020 is based on data up until June, and a fixed estimate is used thereafter. This is the monthly equivalent of https://zenodo.org/record/3951601#.XxYBsihKhPY for this time period. Funding was provided by the European Union’s Horizon 2020 Research and Innovation Programme under grant agreement nos. 820829 (CONSTRAIN) http://constrain-eu.org/ see https://github.com/Priestley-Centre/COVID19_emissions for more details.
description: Note that the data and normalisation process used in the aviation data is subtly updated since the version 4 found in related databases, hence that is referred to as v4.5. It still does not cover the whole month of July, due to publication date. The whole dataset is now considered version 4.5.1 as it features more variables and differently cropped timeframes, however is still consistent with version 4.5 in terms of the input data.
DOI: 10.5281/zenodo.4048824
title: Dynamic Contrast Enhanced MRI Raw Data Acquired with 3D Cones Trajectory

description: This repository contains the raw data for the second dynamic contrast enhanced (DCE) MRI in Extreme MRI: Large-Scale Volumetric Dynamic Imaging from Continuous Non-Gated Acquisitions. The data is stored as numpy arrays, containing k-space data (ksp.npy), coordinates (coord.npy), and density compensation factors (dcf.npy). Code to process and reconstruct the data is available here: https://github.com/mikgroup/extreme_mri For more information about how the data is acquired, please see the linked paper.
description: {"references": ["Dataset associated with arXiv:1909.13482"]}
DOI: 10.5281/zenodo.3647819
title: Dynamic Contrast Enhanced MRI Raw Data Acquired with 3D Cones Trajectory

description: This repository contains the raw data for the second dynamic contrast enhanced (DCE) MRI in Extreme MRI: Large-Scale Volumetric Dynamic Imaging from Continuous Non-Gated Acquisitions. The data is stored as numpy arrays, containing k-space data (ksp.npy), coordinates (coord.npy), and density compensation factors (dcf.npy). Code to process and reconstruct the data is available here: https://github.com/mikgroup/extreme_mri For more information about how the data is acquired, please see the linked paper.
description: {"references": ["Dataset associated with arXiv:1909.13482"]}
DOI: 10.6084/m9.figshare.13003199
title: Set 1_S2_molecule

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003199.v1
title: Set 1_S2_molecule

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.17609/jy7g-6853
title: US and Canada Public Pension System Data 2008-2018

description: This dataset comprises eleven years of historical data (2008 through 2018) for the 25 largest U.S. public pension plans and the ten largest Canadian public pension plans.
DOI: 10.6084/m9.figshare.13003271
title: Set 1_S2_raw_gene

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003271.v1
title: Set 1_S2_raw_gene

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003310.v1
title: Set 1_S2_web_summary

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003310
title: Set 1_S2_web_summary

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.21227/vgz0-mk57
title: Experimental database for detecting and diagnosing rotor broken bar in a three-phase induction motor.

description: The data set contains electrical and mechanical signals from experiments on three-phase induction motors. The experimental tests were carried out for different mechanical loads on the induction motor axis and different severities of broken bar defects in the motor rotor, including data regarding the rotor without defects. Ten repetitions were performed for each experimental condition.
DOI: 10.6084/m9.figshare.12998894
title: R0230_20181024a_videos

description: Rat 0230, skilled reaching data collected in Leventhal laboratory by Alexandra Bova
DOI: 10.6084/m9.figshare.13003316
title: Set 2_R3_metrics

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003316.v1
title: Set 2_R3_metrics

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.5066/p9siao0o
title: Presence and prevalence of pathogens among amphibians of Catoctin Mountain Park, 2014

description: Data described herein was collected by USGS personnel and the project funded by USGS and the National Park Service (Catoctin Mountain Park) through a FY14 NRPP project involving both agencies and developed to detect the presence and prevalence of ranavirus and chytrid pathogens among amphibians of Catoctin Mountain Park (CATO). Supplemental molecular analyses were performed on behalf of LSC by the molecular biology laboratory at Hagerstown Community College whereby students performed the molecular diagnostic testing and provided the raw data to LSC for analysis. There is no data sharing agreement specifying ownership, but the data was presented to the NPS CATO staff to help guide their management decision-making related to amphibians and disease susceptibility. This body of data is stored in spreadsheet format.
DOI: 10.6084/m9.figshare.13003322
title: Set 2_R3_molecule

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003322.v1
title: Set 2_R3_molecule

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003313
title: Set 2_R3_filtered_gene

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003313.v2
title: Set 2_R3_filtered_gene

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003313.v1
title: Set 1_R3_filtered_gene

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003337
title: Set 2_R3_raw_gene

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.6084/m9.figshare.13003337.v1
title: Set 2_R3_raw_gene

description: Renal artery stenosis (RAS) engenders stenotic-kidney ischemia, dysfunction, and injury, but whether these are mediated by cellular senescence has not been elucidated. Using INK-ATTAC transgenic mice, high-resolution imaging, and unbiased scRNA-sequencing of murine kidneys, the authors identified cellular senescence as an important mechanism of progressive injury triggered in renal epithelial/stromal cells within post-stenotic kidneys. Both P16-specific and broad quercetin/dasatinib interventions to blunt senescence improved renal function and structure, underscoring its central role in the pathogenesis of the disease. Furthermore, this mechanism was conserved in human subjects with RAS. These observations reveal new mechanisms that contribute to the pathogenesis of chronic ischemic renal injury, and support development of senolytic therapy to reduce senescent cell burden and delay renal injury.
DOI: 10.5517/ccdc.csd.cc25h0c2
title: CCDC 2010423: Experimental Crystal Structure Determination

description: Related Article: Dmitri V. Konarev, Leokadiya V. Zorina, Salavat S. Khasanov, Rimma N. Lyubovskaya|2020|Dyes Pigm.|184|108769|doi:10.1016/j.dyepig.2020.108769
DOI: 10.5517/ccdc.csd.cc25h0d3
title: CCDC 2010424: Experimental Crystal Structure Determination

description: Related Article: Dmitri V. Konarev, Leokadiya V. Zorina, Salavat S. Khasanov, Rimma N. Lyubovskaya|2020|Dyes Pigm.|184|108769|doi:10.1016/j.dyepig.2020.108769
DOI: 10.5517/ccdc.csd.cc25h0f4
title: CCDC 2010425: Experimental Crystal Structure Determination

description: Related Article: Dmitri V. Konarev, Leokadiya V. Zorina, Salavat S. Khasanov, Rimma N. Lyubovskaya|2020|Dyes Pigm.|184|108769|doi:10.1016/j.dyepig.2020.108769
DOI: 10.5517/ccdc.csd.cc25h0g5
title: CCDC 2010426: Experimental Crystal Structure Determination

description: Related Article: Dmitri V. Konarev, Leokadiya V. Zorina, Salavat S. Khasanov, Rimma N. Lyubovskaya|2020|Dyes Pigm.|184|108769|doi:10.1016/j.dyepig.2020.108769
DOI: 10.5517/ccdc.csd.cc25h0h6
title: CCDC 2010427: Experimental Crystal Structure Determination

description: Related Article: Dmitri V. Konarev, Leokadiya V. Zorina, Salavat S. Khasanov, Rimma N. Lyubovskaya|2020|Dyes Pigm.|184|108769|doi:10.1016/j.dyepig.2020.108769
DOI: 10.5517/ccdc.csd.cc25h0k8
title: CCDC 2010429: Experimental Crystal Structure Determination

description: Related Article: Dmitri V. Konarev, Leokadiya V. Zorina, Salavat S. Khasanov, Rimma N. Lyubovskaya|2020|Dyes Pigm.|184|108769|doi:10.1016/j.dyepig.2020.108769