cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.4040851
title: PowNet-Thailand: Network-constrained Unit Commitment / Economic Dispatch model for the Thai power system with sample data

description: PowNet-Thailand is an implementation of PowNet model on the Thai power system. The model is developed based on the load (domestic and exports) and infrastructure (power plants, substations, and high-voltage transmission lines) of the Thai power system operated in 2016, including a number of Laotian hydro and thermal power plants that supply to Thailand. The power systems’ data are mostly collected from publicly available reports, published by Electricity Generating Authority of Thailand (EGAT), Energy Policy and Planning Office (EPPO) – Thai Ministry of Energy, Electricite Du Laos (EDL), and the Department of Energy Policy and Planning (DEPP) – Laotian Ministry of Energy and Mine. The hydropower budget are simulated with VIC-Res. Please refer to Chowdhury et al. (2020a) for additional details on the power system and model setup. For 2016, the repository contains input data, output data, and a Python script for a sample analysis. In addition, climate-dependent input data (e.g., hydropower budget) for a 30-year (1976-2005) simulation period, used in Chowdhury et al. (2020a), are also provided. Outputs for any of these years can be obtained by running PowNet-Thailand through the following two steps: (1) change simulation year in ‘pownet_thai_datasetup.py’, and (2) run ‘pownet_thai_solver.py’. The basic functionalities and input-output structure of PowNet are described in Chowdhury et al. (2020b). Step-by-step instructions on how to run and customize PowNet for any power system are provided in this GitHub repository. If you use PowNet-Thailand and/or the data for your research, please cite the following papers: Chowdhury, A.K., Dang, T.D., Nguyen, H.T., Koh, R., and Galelli, S., (2020a). The Greater Mekong's climate-water-energy nexus: how ENSO-triggered regional droughts affect power supply and CO<sub>2</sub> emissions. Submitted to Earth’s Future, DOI: https://doi.org/10.1002/essoar.10504393.1. Chowdhury, A.K., Kern, J., Dang, T.D. and Galelli, S., (2020b). PowNet: A Network-Constrained Unit Commitment/Economic Dispatch Model for Large-Scale Power Systems Analysis. Journal of Open Research Software, 8(1), p.5. DOI: http://doi.org/10.5334/jors.302.
DOI: 10.34740/kaggle/dsv/1513180
title: COVID-19 cases by Continent
DOI: 10.6084/m9.figshare.13003070.v1
title: Set 1_R2_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.13003070
title: Set 1_R2_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.13003118.v1
title: Set 1_R2_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.13003118
title: Set 1_R2_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.13003130
title: Set 1_R2_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.13003130.v1
title: Set 1_R2_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.13003139
title: Set 1_S1_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.13003139.v1
title: Set 1_S1_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.13003145
title: Set 1_S1_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.13003145.v1
title: Set 1_S1_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: 10.5517/ccdc.csd.cc2534k0
title: CCDC 1999021: Experimental Crystal Structure Determination

description: Related Article: Christin Kirst, Marco Reichel, Konstantin Karaghiosoff|2021|Inorg.Chim.Acta|514|119951|doi:10.1016/j.ica.2020.119951
DOI: 10.5517/ccdc.csd.cc2534l1
title: CCDC 1999022: Experimental Crystal Structure Determination

description: Related Article: Christin Kirst, Marco Reichel, Konstantin Karaghiosoff|2021|Inorg.Chim.Acta|514|119951|doi:10.1016/j.ica.2020.119951
DOI: 10.5517/ccdc.csd.cc2534m2
title: CCDC 1999023: Experimental Crystal Structure Determination

description: Related Article: Christin Kirst, Marco Reichel, Konstantin Karaghiosoff|2021|Inorg.Chim.Acta|514|119951|doi:10.1016/j.ica.2020.119951
DOI: 10.5517/ccdc.csd.cc2534n3
title: CCDC 1999024: Experimental Crystal Structure Determination

description: Related Article: Christin Kirst, Marco Reichel, Konstantin Karaghiosoff|2021|Inorg.Chim.Acta|514|119951|doi:10.1016/j.ica.2020.119951
DOI: 10.5517/ccdc.csd.cc1n87rx
title: CCDC 1527269: Experimental Crystal Structure Determination

description: Related Article: Rui-Ning Li, Xiao-Hai Guo, Zhe-Yang Wang, Heping Jiang, Lindong Luan, Ming-Xing Li, Xiang He|2021|Inorg.Chim.Acta|514|119986|doi:10.1016/j.ica.2020.119986
DOI: 10.5517/ccdc.csd.cc1n87nt
title: CCDC 1527266: Experimental Crystal Structure Determination

description: Related Article: Rui-Ning Li, Xiao-Hai Guo, Zhe-Yang Wang, Heping Jiang, Lindong Luan, Ming-Xing Li, Xiang He|2021|Inorg.Chim.Acta|514|119986|doi:10.1016/j.ica.2020.119986
DOI: 10.5517/ccdc.csd.cc1n87ms
title: CCDC 1527265: Experimental Crystal Structure Determination

description: Related Article: Rui-Ning Li, Xiao-Hai Guo, Zhe-Yang Wang, Heping Jiang, Lindong Luan, Ming-Xing Li, Xiang He|2021|Inorg.Chim.Acta|514|119986|doi:10.1016/j.ica.2020.119986
DOI: 10.5517/ccdc.csd.cc1n87sy
title: CCDC 1527270: Experimental Crystal Structure Determination

description: Related Article: Rui-Ning Li, Xiao-Hai Guo, Zhe-Yang Wang, Heping Jiang, Lindong Luan, Ming-Xing Li, Xiang He|2021|Inorg.Chim.Acta|514|119986|doi:10.1016/j.ica.2020.119986
DOI: 10.5517/ccdc.csd.cc22frjt
title: CCDC 1919846: Experimental Crystal Structure Determination

description: Related Article: Souad Dgachi, Mark M. Turnbull, Francesco Mezzadri, Alexander J. Norquist, Albert Soran, Jaurrsup Boonmak, Gabriela Nemes, Houcine Naïli|2021|Inorg.Chim.Acta|514|119997|doi:10.1016/j.ica.2020.119997
DOI: 10.5517/ccdc.csd.cc25g2h7
title: CCDC 2009528: Experimental Crystal Structure Determination

description: Related Article: Souad Dgachi, Mark M. Turnbull, Francesco Mezzadri, Alexander J. Norquist, Albert Soran, Jaurrsup Boonmak, Gabriela Nemes, Houcine Naïli|2021|Inorg.Chim.Acta|514|119997|doi:10.1016/j.ica.2020.119997
DOI: 10.5517/ccdc.csd.cc25919v
title: CCDC 2004686: Experimental Crystal Structure Determination

description: Related Article: Shuting Liu, Jingjing Lu, Xiao-Lei Li, Zhenhua Zhu, Jinkui Tang|2020|Dalton Trans.|49|12372|doi:10.1039/D0DT02451A
DOI: 10.5517/ccdc.csd.cc2591bw
title: CCDC 2004687: Experimental Crystal Structure Determination

description: Related Article: Shuting Liu, Jingjing Lu, Xiao-Lei Li, Zhenhua Zhu, Jinkui Tang|2020|Dalton Trans.|49|12372|doi:10.1039/D0DT02451A
DOI: 10.5517/ccdc.csd.cc2591cx
title: CCDC 2004688: Experimental Crystal Structure Determination

description: Related Article: Shuting Liu, Jingjing Lu, Xiao-Lei Li, Zhenhua Zhu, Jinkui Tang|2020|Dalton Trans.|49|12372|doi:10.1039/D0DT02451A
DOI: 10.5517/ccdc.csd.cc2591dy
title: CCDC 2004689: Experimental Crystal Structure Determination

description: Related Article: Shuting Liu, Jingjing Lu, Xiao-Lei Li, Zhenhua Zhu, Jinkui Tang|2020|Dalton Trans.|49|12372|doi:10.1039/D0DT02451A
DOI: 10.5517/ccdc.csd.cc25vqwn
title: CCDC 2021692: Experimental Crystal Structure Determination

description: Related Article: Zijie Qiu, Sobi Asako, Yunbin Hu, Cheng-Wei Ju, Thomas Liu, Loïc Rondin, Dieter Schollmeyer, Jean-Sébastien Lauret, Klaus Müllen, Akimitsu Narita|2020|J.Am.Chem.Soc.|142|14814|doi:10.1021/jacs.0c05504
DOI: 10.34740/kaggle/dsv/1513191
title: Aspect Extraction Portuguese
DOI: 10.6084/m9.figshare.13003148
title: Set 1_S1_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.13003148.v1
title: Set 1_S1_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: 10.7910/dvn/abfnsq/qsdbdl
title: federal_candidates.tab

description: dataset
DOI: 10.7910/dvn/abfnsq/tvse9t
title: README 2019-04-27.rtf

description: readme
DOI: 10.7910/dvn/abfnsq/spdb6a
title: federal_candidates-1.tab

description: :unav
DOI: 10.7910/dvn/abfnsq/vt3mdb
title: federal_candidates.tab

description: :unav
DOI: 10.7910/dvn/abfnsq/vqktew
title: README 2019-04-27.rtf

description: :unav
DOI: 10.7910/dvn/abfnsq/uuppau
title: federal_candidates.tab

description: :unav
DOI: 10.6084/m9.figshare.13003169.v1
title: Set 1_S1_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.13003169
title: Set 1_S1_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.13003172
title: Set 1_S1_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.13003172.v1
title: Set 1_S1_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.13003190
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.