cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.35092/yhjc.12084987.v1
title: Supplementary Figure 2 - Endometrial stromal cells - Genomic annotation of GATA2 and PGR ChIPseq

description: Cistromic analysis revealed similar genome-wide binding of GATA2 to promoter regions in both Veh and IVD-treated cells.<br>Supplementary dataset supporting manuscript currently under review.<br>Abstract: The transcription factor GATA2 is important for endometrial stromal cell decidualization in early pregnancy. Progesterone receptor (PGR) is also critical during decidualization but its interaction with GATA2 in regulating genes and pathways necessary for decidualization in human endometrium are unclear. RNA-sequencing (RNA-seq) was performed to compare gene expression profiles (n=3) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) using an antibody against GATA2 (n=2) was performed to examine binding to target genes in human endometrial stromal cells undergoing in vitro decidualization (IVD including estrogen, progestin and cAMP analogue) or vehicle treatment. We identified 1232 differentially expressed genes (DEGs) in IVD vs. vehicle. GATA2 cistrome in IVD-treated cells was enriched with motifs for GATA, ATF, and JUN, and gene ontology analysis of GATA2 cistrome revealed pathways that regulate cholesterol storage, p38 MAPK and the c-Jun N-terminal kinase cascades. Integration of RNA-seq and ChIP-seq data revealed that the PGR motif is highly enriched at GATA2 binding regions surrounding upregulated genes in IVD-treated cells. The integration of a mined public PGR cistrome in IVD-treated human endometrial cells with our GATA2 cistrome showed that GATA2 binding was significantly enhanced at PGR-binding regions in IVD vs. vehicle. Interrogating two separate ChIP-seq datasets together with RNA-seq revealed integration of GATA2 and PGR action to co-regulate biologic processes during decidualization of human endometrial stromal cells, specifically via WNT activation and stem cell differentiation pathways. These findings reveal the key pathways that are co-activated by GATA2 and PGR that may be therapeutic targets for supporting implantation and early pregnancy.
DOI: 10.35092/yhjc.12084990
title: Supplementary Figure 1 - Endometrial stromal cells with and without IVD - DEGs

description: Endometrial stromal cells were collected from 3 different women and then treated to induce <i>in vitro</i> decidualization (IVD) or with vehicle (Veh). RNA-seq revealed 1232 differentially expressed genes (DEGs), of which 669 genes were significantly upregulated in IVD compared to Veh cells.<br>Supplementary dataset supporting manuscript currently under review. <br>Abstract: The transcription factor GATA2 is important for endometrial stromal cell decidualization in early pregnancy. Progesterone receptor (PGR) is also critical during decidualization but its interaction with GATA2 in regulating genes and pathways necessary for decidualization in human endometrium are unclear. RNA-sequencing (RNA-seq) was performed to compare gene expression profiles (n=3) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) using an antibody against GATA2 (n=2) was performed to examine binding to target genes in human endometrial stromal cells undergoing in vitro decidualization (IVD including estrogen, progestin and cAMP analogue) or vehicle treatment. We identified 1232 differentially expressed genes (DEGs) in IVD vs. vehicle. GATA2 cistrome in IVD-treated cells was enriched with motifs for GATA, ATF, and JUN, and gene ontology analysis of GATA2 cistrome revealed pathways that regulate cholesterol storage, p38 MAPK and the c-Jun N-terminal kinase cascades. Integration of RNA-seq and ChIP-seq data revealed that the PGR motif is highly enriched at GATA2 binding regions surrounding upregulated genes in IVD-treated cells. The integration of a mined public PGR cistrome in IVD-treated human endometrial cells with our GATA2 cistrome showed that GATA2 binding was significantly enhanced at PGR-binding regions in IVD vs. vehicle. Interrogating two separate ChIP-seq datasets together with RNA-seq revealed integration of GATA2 and PGR action to co-regulate biologic processes during decidualization of human endometrial stromal cells, specifically via WNT activation and stem cell differentiation pathways. These findings reveal the key pathways that are co-activated by GATA2 and PGR that may be therapeutic targets for supporting implantation and early pregnancy.
DOI: 10.35092/yhjc.12084990.v1
title: Supplementary Figure 1 - Endometrial stromal cells with and without IVD - DEGs

description: Endometrial stromal cells were collected from 3 different women and then treated to induce <i>in vitro</i> decidualization (IVD) or with vehicle (Veh). RNA-seq revealed 1232 differentially expressed genes (DEGs), of which 669 genes were significantly upregulated in IVD compared to Veh cells.<br>Supplementary dataset supporting manuscript currently under review. <br>Abstract: The transcription factor GATA2 is important for endometrial stromal cell decidualization in early pregnancy. Progesterone receptor (PGR) is also critical during decidualization but its interaction with GATA2 in regulating genes and pathways necessary for decidualization in human endometrium are unclear. RNA-sequencing (RNA-seq) was performed to compare gene expression profiles (n=3) and chromatin immunoprecipitation followed by sequencing (ChIP-seq) using an antibody against GATA2 (n=2) was performed to examine binding to target genes in human endometrial stromal cells undergoing in vitro decidualization (IVD including estrogen, progestin and cAMP analogue) or vehicle treatment. We identified 1232 differentially expressed genes (DEGs) in IVD vs. vehicle. GATA2 cistrome in IVD-treated cells was enriched with motifs for GATA, ATF, and JUN, and gene ontology analysis of GATA2 cistrome revealed pathways that regulate cholesterol storage, p38 MAPK and the c-Jun N-terminal kinase cascades. Integration of RNA-seq and ChIP-seq data revealed that the PGR motif is highly enriched at GATA2 binding regions surrounding upregulated genes in IVD-treated cells. The integration of a mined public PGR cistrome in IVD-treated human endometrial cells with our GATA2 cistrome showed that GATA2 binding was significantly enhanced at PGR-binding regions in IVD vs. vehicle. Interrogating two separate ChIP-seq datasets together with RNA-seq revealed integration of GATA2 and PGR action to co-regulate biologic processes during decidualization of human endometrial stromal cells, specifically via WNT activation and stem cell differentiation pathways. These findings reveal the key pathways that are co-activated by GATA2 and PGR that may be therapeutic targets for supporting implantation and early pregnancy.
DOI: 10.35092/yhjc.12098397
title: Test Sample - DIPY Processed Parkinson's Progression Markers Initiative (PPMI) Data Derivatives

description: This is a small test sample data for Parkinson's Progression Markers Initiative (PPMI) data derivatives. It includes white matter tracts in common space (MNI space) and tracts in the subject's original space. It also includes anatomical measures extracted from diffusion data such as FA, RD, MD, AD for 5 patient subjects and 5 control subjects.<br>Data was processed using DIPY.<br>This data set was generated by Chandio, B.Q., <i>et al.</i> Bundle analytics, a computational framework for investigating the shapes and profiles of brain pathways across populations. <i>Sci Rep</i> <b>10, </b>17149 (2020) paper.<br>Read paper here: https://rdcu.be/b8rUr<br>
DOI: 10.35092/yhjc.12098397.v1
title: DIPY Processed Parkinson's Progression Markers Initiative (PPMI) Data Derivatives - Test Sample

description: This is a small test sample data for Parkinson's Progression Markers Initiative (PPMI) data derivatives. It includes white matter tracts in common space (MNI space) and tracts in the subject's original space. It also includes anatomical measures extracted from diffusion data such as FA, RD, MD, AD for 5 patient subjects and 5 control subjects.<br>Data was processed using DIPY.<br><br>
DOI: 10.35092/yhjc.12111570
title: Clinical benefit of remdesivir in rhesus macaques infected with SARS-CoV-2

description: <b>Background:</b> Effective therapeutics to treat COVID-19 are urgently needed. Remdesivir is a nucleotide prodrug with in vitro and in vivo efficacy against coronaviruses. Here, we tested the efficacy of remdesivir treatment in a rhesus macaque model of SARS-CoV-2 infection. <b>Methods:</b> To evaluate the effect of remdesivir treatment on SARS-CoV-2 disease outcome, we used the recently established rhesus macaque model of SARS-CoV-2 infection that results in transient lower respiratory tract disease. Two groups of six rhesus macaques were infected with SARS-CoV-2 and treated with intravenous remdesivir or an equal volume of vehicle solution once daily. Clinical, virological and histological parameters were assessed regularly during the study and at necropsy to determine treatment efficacy. <b>Results:</b> In contrast to vehicle-treated animals, animals treated with remdesivir did not show signs of respiratory disease and had reduced pulmonary infiltrates on radiographs. Virus titers in bronchoalveolar lavages were significantly reduced as early as 12hrs after the first treatment was administered. At necropsy on day 7 after inoculation, lung viral loads of remdesivir-treated animals were significantly lower and there was a clear reduction in damage to the lung tissue. <b>Conclusions: </b>Therapeutic remdesivir treatment initiated early during infection has a clear clinical benefit in SARS-CoV-2-infected rhesus macaques. These data support early remdesivir treatment initiation in COVID-19 patients to prevent progression to severe pneumonia.<br><br>Dataset supports publication:Williamson, B.N., Feldmann, F., Schwarz, B. et al. Clinical benefit of remdesivir in rhesus macaques infected with SARS-CoV-2. Nature (2020). https://doi.org/10.1038/s41586-020-2423-5<br><br>Also previously shared on bioRxiv: https://doi.org/10.1101/2020.04.15.043166
DOI: 10.35092/yhjc.12111570.v1
title: Clinical benefit of remdesivir in rhesus macaques infected with SARS-CoV-2

description: <b>Background:</b> Effective therapeutics to treat COVID-19 are urgently needed. Remdesivir is a nucleotide prodrug with in vitro and in vivo efficacy against coronaviruses. Here, we tested the efficacy of remdesivir treatment in a rhesus macaque model of SARS-CoV-2 infection. <b>Methods:</b> To evaluate the effect of remdesivir treatment on SARS-CoV-2 disease outcome, we used the recently established rhesus macaque model of SARS-CoV-2 infection that results in transient lower respiratory tract disease. Two groups of six rhesus macaques were infected with SARS-CoV-2 and treated with intravenous remdesivir or an equal volume of vehicle solution once daily. Clinical, virological and histological parameters were assessed regularly during the study and at necropsy to determine treatment efficacy. <b>Results:</b> In contrast to vehicle-treated animals, animals treated with remdesivir did not show signs of respiratory disease and had reduced pulmonary infiltrates on radiographs. Virus titers in bronchoalveolar lavages were significantly reduced as early as 12hrs after the first treatment was administered. At necropsy on day 7 after inoculation, lung viral loads of remdesivir-treated animals were significantly lower and there was a clear reduction in damage to the lung tissue. <b>Conclusions:</b> Therapeutic remdesivir treatment initiated early during infection has a clear clinical benefit in SARS-CoV-2-infected rhesus macaques. These data support early remdesivir treatment initiation in COVID-19 patients to prevent progression to severe pneumonia.
DOI: 10.35092/yhjc.12133509
title: All Behavior data to reproduce Figures 1 through Supplementary Figure 5 and Table 1 in "The central amygdala recruits mesocorticolimbic circuitry for pursuit of sugar, cocaine, or pain"

description: This dataset contains behavioral data collected from each experiment in above-title paper. Experiments involved optogenetically stimulating CeA (ChR2) during reward choice tasks and during interaction with a shock-delivering rod in rats.<br><br>Dataset supporting: Warlow, S.M., Naffziger, E.E. & Berridge, K.C. The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain. <i>Nat Commun</i> <b>11</b>, 2716 (2020). https:/doi.org/10.1038/241467-020-16407-1<br><br>Abstract: How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions were created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. Pairings made the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruited mesocorticolimbic incentive-related circuitry. Shock-associated cues also gained positive incentive value and were pursued. Yet the motivational effects of paired CeA stimulation could be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increased defensive reactions. Finally, CeA ChR2 valence could be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.<br><br>Find other related resources in the collection here: https://doi.org/10.35092/yhjc.c.4939542
DOI: 10.35092/yhjc.12133509.v1
title: All Behavior data to reproduce Figures 1 through Supplementary Figure 5 and Table 1 in "The central amygdala recruits mesocorticolimbic circuitry for pursuit of sugar, cocaine, or pain"

description: This dataset contains behavioral data collected from each experiment in above-title paper. Experiments involved optogenetically stimulating CeA (ChR2) during reward choice tasks and during interaction with a shock-delivering rod in rats.<br><br>Dataset supporting: Warlow, S.M., Naffziger, E.E. & Berridge, K.C. The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain. <i>Nat Commun</i> <b>11</b>, 2716 (2020). https:/doi.org/10.1038/241467-020-16407-1<br><br>Abstract: How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions were created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. Pairings made the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruited mesocorticolimbic incentive-related circuitry. Shock-associated cues also gained positive incentive value and were pursued. Yet the motivational effects of paired CeA stimulation could be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increased defensive reactions. Finally, CeA ChR2 valence could be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.<br><br>Find other related resources in the collection here: https://doi.org/10.35092/yhjc.c.4939542
DOI: 10.35092/yhjc.12133521
title: CeA ChR2 Virus Expression Mapping and quantification

description: This data quantifies the spread of ChR2 Virus injections into CeA, spread around the implanted fiber optic tip.<br><br>Dataset supporting: Warlow, S.M., Naffziger, E.E. & Berridge, K.C. The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain. <i>Nat Commun</i> <b>11</b>, 2716 (2020). https:/doi.org/10.1038/241467-020-16407-1<br><br>Abstract: How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions were created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. Pairings made the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruited mesocorticolimbic incentive-related circuitry. Shock-associated cues also gained positive incentive value and were pursued. Yet the motivational effects of paired CeA stimulation could be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increased defensive reactions. Finally, CeA ChR2 valence could be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.<br><br>Find other related resources in the collection here: https://doi.org/10.35092/yhjc.c.4939542
DOI: 10.35092/yhjc.12133521.v1
title: CeA ChR2 Virus Expression Mapping and quantification

description: This data quantifies the spread of ChR2 Virus injections into CeA, spread around the implanted fiber optic tip.<br><br>Dataset supporting: Warlow, S.M., Naffziger, E.E. & Berridge, K.C. The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain. <i>Nat Commun</i> <b>11</b>, 2716 (2020). https:/doi.org/10.1038/241467-020-16407-1<br><br>Abstract: How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions were created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. Pairings made the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruited mesocorticolimbic incentive-related circuitry. Shock-associated cues also gained positive incentive value and were pursued. Yet the motivational effects of paired CeA stimulation could be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increased defensive reactions. Finally, CeA ChR2 valence could be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.<br><br>Find other related resources in the collection here: https://doi.org/10.35092/yhjc.c.4939542
DOI: 10.35092/yhjc.12133536
title: CeA ChR2 Fos Plume worksheet

description: This data set shows how the spread Fos protein expression away from the fiber optic tip was quantified, and shows Fos protein levels within CeA between ChR2 and eYFP control rats among various conditions - after passive laser stimulation, after earning sucrose or cocaine paired with stimulation, or after interacting with a shock-delivering rod.<br><br>Dataset supporting: Warlow, S.M., Naffziger, E.E. & Berridge, K.C. The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain. <i>Nat Commun</i> <b>11</b>, 2716 (2020). https:/doi.org/10.1038/241467-020-16407-1<br><br>Abstract: How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions were created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. Pairings made the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruited mesocorticolimbic incentive-related circuitry. Shock-associated cues also gained positive incentive value and were pursued. Yet the motivational effects of paired CeA stimulation could be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increased defensive reactions. Finally, CeA ChR2 valence could be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.<br>Find other related resources in the collection here: https://doi.org/10.35092/yhjc.c.4939542<br>
DOI: 10.35092/yhjc.12133536.v1
title: CeA ChR2 Fos Plume worksheet

description: This data set shows how the spread Fos protein expression away from the fiber optic tip was quantified, and shows Fos protein levels within CeA between ChR2 and eYFP control rats among various conditions - after passive laser stimulation, after earning sucrose or cocaine paired with stimulation, or after interacting with a shock-delivering rod.<br><br>Dataset supporting: Warlow, S.M., Naffziger, E.E. & Berridge, K.C. The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain. <i>Nat Commun</i> <b>11</b>, 2716 (2020). https:/doi.org/10.1038/241467-020-16407-1<br><br>Abstract: How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions were created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. Pairings made the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruited mesocorticolimbic incentive-related circuitry. Shock-associated cues also gained positive incentive value and were pursued. Yet the motivational effects of paired CeA stimulation could be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increased defensive reactions. Finally, CeA ChR2 valence could be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.<br>Find other related resources in the collection here: https://doi.org/10.35092/yhjc.c.4939542<br>