cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5517/ccdc.csd.cc25h0l9
title: CCDC 2010430: 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.cc25h7b8
title: CCDC 2010639: Experimental Crystal Structure Determination

description: Related Article: Xiaojuan Wang, Di Gao, Duanxiu Li, Qihuang Xie, Zongwu Deng, Hailu Zhang|2020|Cryst.Growth Des.|20|5664|doi:10.1021/acs.cgd.0c00891
DOI: 10.5517/ccdc.csd.cc25h7c9
title: CCDC 2010640: Experimental Crystal Structure Determination

description: Related Article: Xiaojuan Wang, Di Gao, Duanxiu Li, Qihuang Xie, Zongwu Deng, Hailu Zhang|2020|Cryst.Growth Des.|20|5664|doi:10.1021/acs.cgd.0c00891
DOI: 10.5517/ccdc.csd.cc25fqv6
title: CCDC 2009198: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25fqw7
title: CCDC 2009199: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25frhw
title: CCDC 2009218: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25wvkh
title: CCDC 2022767: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25wvlj
title: CCDC 2022768: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25wvmk
title: CCDC 2022769: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25wvnl
title: CCDC 2022770: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25fqs4
title: CCDC 2009196: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25fqx8
title: CCDC 2009200: Experimental Crystal Structure Determination

description: Related Article: Qiuming Liang, Jack H. Lin, Joshua C. DeMuth, Michael L. Neidig, Datong Song|2020|Dalton Trans.|49|12287|doi:10.1039/D0DT02087G
DOI: 10.5517/ccdc.csd.cc25l2gb
title: CCDC 2013371: Experimental Crystal Structure Determination

description: Related Article: Yongliang Liu, Youying Di, Chengfang Qiao, Mingbao Liu, Chunsheng Zhou|2020|J.Solid State Chem.|292|121688|doi:10.1016/j.jssc.2020.121688
DOI: 10.6084/m9.figshare.13003343.v1
title: Set 2_R4_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.13003343
title: Set 2_R4_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.13003346.v1
title: Set 2_R4_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.13003346
title: Set 2_R4_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.13003349
title: Set 2_R4_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.13003349.v1
title: Set 2_R4_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.13003355
title: Set 2_R4_possorted_genome

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.13003361
title: Set 2_R4_genome 2

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.13003361.v1
title: Set 2_R4_genome 2

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.12998894.v1
title: R0230_20181024a_videos

description: Rat 0230, skilled reaching data collected in Leventhal laboratory by Alexandra Bova
DOI: 10.6084/m9.figshare.13003364
title: Set 2_R4_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: 10.5281/zenodo.4048833
title: Long Timescale X-ray Variability of BAL and mini-BAL quasars

description: Serendipitous and targeted <em>Chandra</em> observations of BAL and mini-BAL quasars identified in SDSS DR16Q. This data set contains 293 observations of 93 BAL and mini-BAL quasars. This data accompanies the research note: Timlin, J., Brandt, W.N., Zhu, S. (2020), RNASS, in press.
DOI: 10.6084/m9.figshare.13003364.v1
title: Set 2_R4_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: 10.5281/zenodo.4041603
title: Long Timescale X-ray Variability of BAL and mini-BAL quasars

description: Serendipitous and targeted <em>Chandra</em> observations of BAL and mini-BAL quasars identified in SDSS DR16Q. This data set contains 293 observations of 93 BAL and mini-BAL quasars. This data accompanies the research note: Timlin, J., Brandt, W.N., Zhu, S. (2020), RNASS, in press.
DOI: 10.6084/m9.figshare.13003367
title: Set 2_S3_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.13003367.v1
title: Set 2_S3_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.13003370.v1
title: Set 2_S3_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.13003370
title: Set 2_S3_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: 10.6073/pasta/9de72a1bc803fd9d22476c2cf1b55c00
title: Sawgrass above ground biomass from the Taylor Slough, Everglades National Park (FCE LTER), South Florida from August 1999 to Present

description: Sawgrass biomass is measured for TS/Ph-1, 2, 3, & 6 since 1999; TS/Ph-4 & 5 since 1997 to 2006; SRS-1b, 2, & 3 since 2000; SRS1c for 2005 to 2006, and SRS1d since 2006. Three 1 m2 plots are placed on each site. The sites are measured every two months. The number of sawgrass plants is counted for each 1 m2 plot and one third or a minimum of fifteen plants is measured. For each measured plant, measurements of the total number of live leaves, length of the live leaves, and culm diameter at the base are taken. From these measurements we calculate the average leaf length, and the sum of the length of the leaves. We created a model for biomass using a stepwise regression to see which of the variables measured and calculated are more correlated to explain plant biomass. Obtaining the mean biomass for the plants within the plot and multiplying it by the number of plants counted in the plot calculates biomass for each plot. The total biomass for each plot is summed with the other two plots in the same site, and they are averaged to obtain one biomass number per site. To validate our model, plant clippings are obtained in which four plants are clipped (small, medium, large, inflorescence) from each site. The same measurements are applied to the clipped plants as those applied to the measured plants in the plots. The plant clippings are oven dried at 70 degrees C and weighed.
DOI: 10.6084/m9.figshare.11663748.v3
title: Sediment Balance in Coastal Louisiana from 2006 to 2015

description: A decadal (2006 to 2015) sediment mass and volume balance for coastal Louisiana from calculated from the Coastwide Reference Monitoring System (CRMS) data using Bayesian kriging.
DOI: 10.6084/m9.figshare.13003376
title: Set 2_S3_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.13003376.v1
title: Set 2_S3_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.13003385
title: Set 2_S3_possorted_genome

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.