Find research datasets worth reusing

opencc-by-4.0Feb 2022View details →

Raw Data for the article: Extracellular Vesicle-Derived microRNAs of Human Wharton's Jelly Mesenchymal Stromal Cells May Activate Endogenous VEGF-A to Promote Angiogenesis

Despite low levels of vascular endothelial growth factor (VEGF)-A, the secretome of human Wharton's jelly (WJ) mesenchymal stromal cells (MSCs) effectively promoted proangiogenic responses in vitro, which were impaired upon the depletion of small (~140 nm) extracellular vesicles (EVs). The isolated EVs shared the low VEGF-A profile of the secretome and expressed five microRNAs, which were upregulated compared to fetal dermal MSC-derived EVs. These upregulated microRNAs exclusively targeted the VEGF-A gene within 54 Gene Ontology (GO) biological processes, 18 of which are associated with angiogenesis. Moreover, 15 microRNAs of WJ-MSC-derived EVs were highly expressed (Ct value ≤ 26) and exclusively targeted the thrombospondin 1 (THBS1) gene within 75 GO biological processes, 30 of which are associated with the regulation of tissue repair. The relationship between predicted microRNA target genes and WJ-MSC-derived EVs was shown by treating human umbilical-vein endothelial cells (HUVECs) with appropriate doses of EVs. The exposure of HUVECs to EVs for 72 h significantly enhanced the release of VEGF-A and THBS1 protein expression compared to untreated control cells. Finally, WJ-MSC-derived EVs stimulated in vitro tube formation along with the migration and proliferation of HUVECs. Our findings can contribute to a better understanding of the molecular mechanisms underlying the proangiogenic responses induced by human umbilical cord-derived MSCs, suggesting a key regulatory role for microRNAs delivered by EVs.

Extended data for "The need to reassess single-cell RNA sequencing datasets: the importance of biological sample processing"

Extended data for "The need to reassess single-cell RNA sequencing datasets: the importance of biological sample processing"

Raw Data for the article: Human Amnion-Derived Mesenchymal Stromal Cells: A New Potential Treatment for Carbapenem-Resistant Enterobacterales in Decompensated Cirrhosis

Background: Spontaneous bacterial peritonitis (SBP) is a severe and often fatal infection in patients with decompensated cirrhosis and ascites. The only cure for SBP is antibiotic therapy, but the emerging problem of bacterial resistance requires novel therapeutic strategies. Human amniotic mesenchymal stromal cells (hA-MSCs) possess immunomodulatory and anti-inflammatory properties that can be harnessed as a therapy in such a context. Methods: An in vitro applications of hA-MSCs in ascitic fluid (AF) of cirrhotic patients, subsequently infected with carbapenem-resistant Enterobacterales, was performed. We evaluated the effects of hA-MSCs on bacterial load, innate immunity factors, and macrophage phenotypic expression. Results: hA-MSCs added to AF significantly reduce the proliferation of both bacterial strains at 24 h and diversely affect M1 and M2 polarization, C3a complement protein, and ficolin 3 concentrations during the course of infection, in a bacterial strain-dependent fashion. Conclusion: This study shows the potential usefulness of hA-MSC in treating ascites infected with carbapenem-resistant bacteria and lays the foundation to further investigate antibacterial and anti-inflammatory roles of hA-MSC in in vivo models.

TestDataset for Oneat networks for detection and prediction of dividing Hela cells for different imaging modalities

Here we present the tif files to be used to test the Oneat networks for detection and prediction of division events for Hela cells imaged under different imaging modalities and presented originally here: https://zenodo.org/record/6139958#.Yjcjl3rMJD8

opencc-zeroMar 2022View details →

dryad36/100

Effects of titanium dioxide nanoparticles on porcine pre-pubertal sertoli cells

This dataset contains data from an in vitro experiment described in the paper: "Mancuso F, Arato I, Di Michele A, Antognelli C, Angelini L, Bellucci C, Lilli C, Boncompagni S, Fusella A, Bartolini D, Russo C, Moretti M, Nocchetti M, Gambelunghe A, Muzi G, Baroni T, Giovagnoli S, Luca G. Effects of Titanium Dioxide Nanoparticles on Porcine Prepubertal Sertoli Cells: An "In Vitro" Study. Front Endocrinol (Lausanne). 2022 Jan 3;12:751915. doi: 10.3389/fendo.2021.751915. PMID: 35046890; PMCID: PMC87623342". The data describes the X-ray diffraction (XRD), scanning electron microscopy (SEM) analysis to confirm the correct synthesis of titanium dioxide nanoparticles (TiO2 NPs), and the transmission electron microscopy (TEM) analysis to investigate the morphological/ultrastructural effects on porcine pre-pubertal Sertoli cells (SCs), after an acute (24 hours) and chronic (from 1 up to 3 weeks) exposure, at both sub-toxic (5 µg/ml) and toxic (100 µg/ml) doses of TiO2 NPs. The diffractogram confirmed the correct synthesis of TiO2 NPs in accordance with the International Centre for Diffraction Data Sample (JCPDS 00-001-0562) and the asterisk (*) represents the peaks of TiO NPs in anatase form; SEM analysis showed that the mean size distribution of TiO2 NPs in dry form was 20 ± 5 nm and confirmed that TiO2 NPs tend to form aggregates of submicrometric dimensions; Representative TEM images of unexposed SCs showed elongated oval or spindle-shaped SCs containing quite large nuclei (N) and abundant mitochondria. SCs did not show substantial and/or severe ultrastructural alterations in SCs treated with 5 µg/ml TiO2 NPs for 1 and 2 weeks, in all the other exposure conditions (5 µg/ml for 3 weeks and 100 µg/ml for 1, 2, and 3 weeks), SCs showed several ultrastructural changes with a high percentage of severely damaged SCs, presenting different features of cell stress such as deeply invaginated and shrunk nuclei, disorder/ marginalization of chromatin components, swollen very fragmented, or almost completely missing endoplasmic reticulum membranes. In addition, mitochondrial morphology was severely affected and mitochondria number dramatically decreased with the presence of several large vacuoles, probably as a result of apoptotic mitochondria and/or enlarged endoplasmic reticulum and/or increased frequency of lipid droplets. The main results of the experiments are that long time constant exposure of SCs at both TiO2 NPs concentrations inevitably led to an altered ultrastructure.

Supporting molecular simulations data for "Pseudo-halide anion engineering for α-FAPbI3 perovskite solar cells"

Supporting molecular simulations data for "Pseudo-halide anion engineering for α-FAPbI3 perovskite solar cells"

RPE-1 GFP-H2B iCas9 sgFBXW7-A cell undergoing mitosis with a lagging chromosome that forms a micronucleus

Zeiss AxioObserver video showing an RPE-1 GFP-H2B iCas9 sgFBXW7-A cell undergoing mitosis with a lagging chromosome that forms a micronucleus. Cells were treated with 1 μg/mL doxycycline for 96 hours to induce Cas9 expression and were imaged every 2 minutes for 24 hours at 40x magnification. At 15:44 chromosomes begin to condense (prophase); at 16:04 chromosomes begin to align on the metaphase plate (prometaphase); at 16:10 the chromosomes are aligned (metaphase); at 16:12 chromosomes are pulled to opposite poles of the cell (anaphase) and the lagging chromosome can be seen above the separating chromosomes; at 16:18 the chromosomes begin to unravel (telophase) and the lagging chromosome can be seen on the left-hand side of the chromosomes of the left daughter cell; from 16:28 onwards the lagging chromosome forms a micronucleus next to the nucleus of the daughter cell.

RPE-1 GFP-H2B iCas9 cells undergoing mitosis

Zeiss AxioObserver video showing RPE-1 GFP-H2B iCas9 cells undergoing mitosis. Cells were treated with 1 μg/mL doxycycline for 96 hours to induce Cas9 expression and were imaged every 2 minutes for 24 hours at 40x magnification.

RPE-1 iCas9 sgNT cells undergoing nocodazole-induced mitotic arrest

Phasefocus LiveCyte video showing RPE-1 iCas9 sgNT cells undergoing nocodazole-induced mitotic arrest. Cells were treated with 1 μg/mL doxycycline for 96 hours to induce Cas9 expression and were imaged every 9 minutes for 48 hours at 20x magnification. From 1:11 cells start entering mitosis as indicated by their rounding up into a ball; from 9:35 mitotic cells begin to slip from mitosis as indicated by rounded mitotic cells flattening. A mitotic cell undergoes mitotic cell death at 42:35 as indicated by the presence of propidium iodide (red) in the top right corner.

RPE-1 GFP-H2B iCas9 cells undergoing nocodazole-induced mitotic arrest

Phasefocus LiveCyte video showing RPE-1 GFP-H2B iCas9 cells undergoing nocodazole-induced mitotic arrest. Cells were treated with 1 μg/mL doxycycline for 96 hours to induce Cas9 expression and were imaged every 9 minutes for 48 hours at 20x magnification. Mitotic cells can be seen from 0:00 as indicated by their rounding up into a ball; from 2:41 mitotic cells begin to slip from mitosis as indicated by rounded mitotic cells flattening. A dead cell can be seen from 0:00 as indicated by the presence of propidium iodide (red) and two other mitotic cells undergo mitotic cell death at 43:42 and 44:20 in the bottom left corner.

RPE-1 GFP-H2B iCas9 cells undergoing paclitaxel-induced mitotic arrest

Phasefocus LiveCyte video showing RPE-1 GFP-H2B iCas9 cells undergoing paclitaxel-induced mitotic arrest. Cells were treated with 1 μg/mL doxycycline for 96 hours to induce Cas9 expression and were imaged every 9 minutes for 48 hours at 20x magnification. From 3:17 cells start entering mitosis as indicated by their rounding up into a ball; from 12:44 mitotic cells begin to either slip from mitosis as indicated by rounded mitotic cells flattening or undergoing mitotic cell death as indicated by the presence of propidium iodide (red).

Object for single-cell mouse HSC development data

This file contains SingleCellExperiment object generated from mouse HSC development data, including raw and log-normalized counts, gene regulatory network inferred by PUIC, transcription factor activity matrix estimated by metaRegulon.

An optimized 4C-seq protocol based on cistrome and epigenome data in the mouse RAW264.7 macrophage cell line

In this protocol, we describe the 4C-seq method in detail using RAW264.7 cells, a mouse macrophage cell line widely used to study acute and metabolic inflammation. We specifically outline how cistrome and epigenome data can be integrated into the primer designing step, critical for the entire protocol. Because intra-TAD chromatin loops are facilitated by transcription factors and coregulators, many of which are co-localized in open chromatin regions, the binding centers of those factors can be obtained by chromatin immunoprecipitation sequencing (ChIP-seq). The binding sites of these factors reflect the coherent loci of the chromatin loops and therefore can be used as references to improve the accuracy of the 4C primers. We specifically describe the 4C protocol using examples of recently identified Ccl2 enhancer and silencer as bait.

Dataset for the paper "High Loading of Single Atomic Iron Sites in Pyrolysed Fe-NC Oxygen Reduction Catalysts for Proton Exchange Membrane Fuel Cells", DOI:10.1038/s41929-022-00772-9

The data in this spreadsheet was used to produce the figures in the paper             Authors:              Asad Mehmood, Mengjun Gong, Frédéric Jaouen, Aaron Roy, Andrea Zitolo, Anastassiya Khan, Moulay-Tahar Sougrati, Mathias Primbs, Alex Martinez Bonastre, Dash Fongalland, Goran Drazic, Peter Strasser, Anthony Kucernak Title:      High Loading of Single Atomic Iron Sites in Pyrolysed Fe-NC Oxygen Reduction Catalysts for Proton Exchange Membrane Fuel Cells Journal: Nature Materials DOI:       10.1038/s41929-022-00772-9 Please cite the above reference if you wish to use this data                           DOI of data:        10.5281/zenodo.6411262

opencc-zeroApr 2022View details →

dryad36/100

Single-Cell RNA-sequencing of neural precursor cells from an Alzheimer's mouse model, wild-type mice, and Alzheimer's mice rescued with Usp16 haploinsufficiency

Alzheimer's disease (AD) is a progressive neurodegenerative disease observed with aging that represents the most common form of dementia. To date, therapies targeting end-stage disease plaques, tangles, or inflammation have limited efficacy. Therefore, we set out to identify an earlier targetable phenotype. Utilizing a mouse model of AD we found that cell intrinsic neural precursor cell (NPC) dysfunction precedes widespread inflammation and amyloid plaque pathology, making it one of the earlier defects in the evolution of the disease. We demonstrate that reversing impaired NPC self-renewal via genetic reduction of USP16, a histone modifier and critical physiological antagonist of the Polycomb Repressor Complex 1, can prevent downstream cognitive defects and decrease astrogliosis in vivo. To delineate potential self-renewal pathways that might contribute to the defect and rescue of Tg-SwDI NPCs and Tg-SwDI/Usp16+/- NPCs, respectively, we performed single-cell RNA-seq and gene set enrichment analysis (GSEA) on lineage depleted primary FACS-sorted CD31-CD45-Ter119-CD24- NPCs from Tg-SwDI, WT, and Tg-SwDI/Usp16+/- mice at 3-4 months and 1 year of age. Using the GSEA Hallmark gene sets, we found only three gene sets that were enriched in Tg-SwDI mice over WT mice and rescued in the Tg-SwDI/Usp16+/- mice at both ages: TGF-ß pathway, oxidative phosphorylation, and Myc Targets. The TGF-ß pathway consistently had the highest normalized enrichment score in pairwise comparisons between Tg-SwDI vs WT and Tg-SwDI vs Tg-SwDI/Usp16+/- of the three rescued pathways. These data suggest that USP16 may regulate neural precursor cell function in part through the BMP pathway.

Investigation the cytotoxicity of newly synthesized quinazo-line–sulfonamide derivatives in human leukemia cell lines and hematopoietic activity in zebrafish embryos.

These videos contain the time lapse imaging of the wild type  zebrafish embryos showing the circulation, control (mock 0.5% V/V DMSO) and compound 4a treated embryos at 72 hours post fertilization. The compound 4a specifically blocked the formation of blood and no circulation was seen in these embryos.

Dynamic deformation calculation of articular cartilage and cells using resonance-driven laser scanning microscopy - Deformable Registration Validation Dataset

This dataset includes the supporting input files, scripts, and output files for validation tests of lsmgridtrack v0.3 applied to resonance scanned images.

Wind and solar capacity factor time series by year and grid cell over the contiguous U.S.

This data set contains hourly capacity factor time series of wind and solar resources over the contiguous U.S.   The included time series cover four individual years and 2,586 grid cells. The years range from 2016 to 2019. The grid cells correspond to the grid cells of the NASA's MERRA-2 reanalysis data set into which the contiguous U.S. is subdivided. The grid cells have a spatial resolution of 0.5° latitude x 0.625° longitude with dimensions ranging from about 55 km x 45 km to 55 km x 62 km.   This data set is used to generate the results of the following journal article: Enrico G. A. Antonini, Tyler H. Ruggles, David J. Farnham, Ken Caldeira, "The quantity-quality transition in the value of expanding wind and solar power generation", iScience 25 (4), 104140, 2022.   Code and instructions required to reproduce the results reported in the above paper are available in the GitHub repositories at <a href="https://github.com/eantonini/Distributed_wind_and_solar_generation">https://github.com/eantonini/Distributed_wind_and_solar_generation</a> and <a href="https://github.com/carnegie/MEM_public/tree/Antonini_et_al_2022">https://github.com/carnegie/MEM_public/tree/Antonini_et_al_2022</a>.

Metabolic data: Inhibition of mitochondrial complex I reverses NOTCH1-driven metabolic reprogramming in T-cell acute lymphoblastic leukemia

T-cell acute lymphoblastic leukemia (T-ALL) is commonly driven by activating mutations in NOTCH1 that facilitate glutamine oxidation. Here we identify oxidative phosphorylation (OxPhos) as a critical pathway for leukemia cell survival and demonstrate a direct relationship between NOTCH1, elevated OxPhos gene expression, and acquired chemoresistance in pre-leukemic and leukemic models. Disrupting OxPhos with IACS-010759, an inhibitor of mitochondrial complex I, causes potent growth inhibition through induction of metabolic shut-down and redox imbalance in NOTCH1-mutated and less so in NOTCH1-wt T-ALL cells. Mechanistically, inhibition of OxPhos induces metabolic reprogramming into glutaminolysis. We show that pharmacological blockade of OxPhos combined with inducible knock-down of glutaminase, the key glutamine enzyme, confers synthetic lethality in mice harboring NOTCH1-mutated T-ALL. We leverage this synthetic lethal interaction to demonstrate that IACS-010759 in combination with chemotherapy containing L-asparaginase, an enzyme that uncovers the glutamine dependency of leukemic cells, causes reduced glutaminolysis and profound tumor reduction in pre-clinical models of human T-ALL. In summary, this metabolic dependency of T-ALL on OxPhos provides a rational therapeutic target.