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2,706 results for “Mouse model”
In vivo T1w MRI of a TDP-43 knock-in mouse model of ALS-FTD
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Hydrogen sulfide release via the ACE inhibitor Zofenopril prevents intimal hyperplasia in human vein segments and in a mouse model of carotid artery stenosis
<p>The current strategies to reduce intimal hyperplasia (IH) principally rely on local drug delivery, in endovascular approach. The oral angiotensin converting enzyme inhibitor (ACEi) Zofenopril has additional effects compared to other non-sulfyhydrated ACEi to prevent intimal hyperplasia and restenosis. Given the number of patients treated with ACEi worldwide, these findings call for further prospective clinical trials to test the benefits of sulfhydrated ACEi over classic ACEi for the prevention of restenosis in hypertensive patients.</p> <p>Abstract</p> <p>Objectives</p> <p>Hypertension is a major risk factor for intimal hyperplasia (IH) and restenosis following vascular and endovascular interventions. Pre-clinical studies suggest that hydrogen sulfide (H2S), an endogenous gasotransmitter, limits restenosis. While there is no clinically available pure H2S releasing compound, the sulfhydryl-containing angiotensin-converting enzyme inhibitor Zofenopril is a source of H2S. Here, we hypothesized that Zofenopril, due to H2S release, would be superior to other non-sulfhydryl containing angiotensin converting enzyme inhibitor (ACEi), in reducing intimal hyperplasia in the context of hypertension.</p> <p>Materials</p> <p>Spontaneously hypertensive male Cx40 deleted mice (Cx40-/-) or WT littermates were randomly treated with Enalapril 20 mg (Mepha Pharma) or Zofenopril 30 mg (Mylan SA). Discarded human vein segments and primary human smooth muscle cells (SMC) were treated with the active compound Enalaprilat or Zofenoprilat.</p> <p>Methods</p> <p>IH was evaluated in mice 28 days after focal carotid artery stenosis surgery and in human vein segments cultured for 7 days ex vivo. Human primary smooth muscle cell (SMC) proliferation and migration were studied in vitro.</p> <p>Results</p> <p>Compared to control animals (intima/media thickness=2.3±0.33), Enalapril reduced IH in Cx40-/- hypertensive mice by 30% (1.7±0.35; p=0.037), while Zofenopril abrogated IH (0.4±0.16; p<.0015 vs. Ctrl and p>0.99 vs. sham-operated Cx40-/-mice). In WT normotensive mice, enalapril had no effect (0.9665±0.2 in control vs 1.140±0.27; p>.99), while Zofenopril also abrogated IH (0.1623±0.07, p<.008 vs. Ctrl and p>0.99 vs. sham-operated WT mice). Zofenoprilat, but not Enalaprilat, also prevented intimal hyperplasia in human veins segments ex vivo. The effect of Zofenopril on carotid and SMC correlated with reduced SMC proliferation and migration. Zofenoprilat inhibited the MAPK and mTOR pathways in SMC and human vein segments.</p> <p>Conclusion</p> <p>Zofenopril provides extra beneficial effects compared to non-sulfhydryl ACEi to reduce SMC proliferation and restenosis, even in normotensive animals. These findings may hold broad clinical implications for patients suffering from vascular occlusive diseases and hypertension.</p>
DATA to support Dyrk1a function in glutamatergic neurons in mouse models of Mental Retardation Disease 7 (MRD7) and Down syndrome (or trisomy 21)
<p>Four datasets are provided here to support the function of Dyrk1a in glutamatergic neurons in mouse models of Mental Retardation Disease 7 (MRD7) and Down syndrome (or trisomy 21):</p> <p>- RNAseq data to compare hippocampal expressed genes at postnatal day 30, in the complete inactivation of Dyrk1a in glutamatergic neurons using a Dyrk1a floxed-allele and the Camk2:Cre transgene</p> <p>- data from all the figures</p> <p>-data from all the supplementary figures </p> <p>-data from the quantitative proteomic analysis made from hippocampal extract of wt, Dyrk1a heterozygote, Dp(16)1Yey and Dp(16)1Yey with only two functional copies of Dyrk1a</p> <p>Detailed information are available in the article by Brault et al 2021, deposited in Biorachiv https://doi.org/10.1101/2021.05.01.442242 </p>
Data from: Chronic Rapamycin administration via drinking water mitigates the pathological phenotype in a Krabbe disease mouse model through autophagy activation.
<p>ABSTRACT </p><p>Krabbe disease (KD) is a rare disorder caused by a deficiency of the lysosomal enzyme galactosylceramidase (GALC), resulting in the accumulation of the cytotoxic metabolite psychosine (PSY) in the nervous system. This accumulation triggers demyelination and neurodegeneration. Despite ongoing research, the underlying pathogenic mechanisms remain incompletely understood, and there is currently no cure available.</p><p>Previous studies from our lab revealed the presence of autophagy dysfunctions in KD pathogenesis, as evidenced by the presence of p62-tagged protein aggregates in the brains of KD mice and increased p62 levels in the KD sciatic nerve. We also demonstrated that the autophagy inducer Rapamycin (RAPA) can partially restore the wild-type (WT) phenotype in KD primary cells by reducing the number of p62 aggregates.</p><p>In this study, we tested RAPA in the Twitcher (TWI) mouse, a spontaneous KD mouse model. We administered the drug ad libitum via drinking water (15 mg/L) starting from post-natal day (PND) 21-23. We longitudinally monitored the motor performance of the mice through grip strength and rotarod tests, along with various biochemical parameters related to KD pathogenesis (i.e. autophagy markers expression, myelination, astrogliosis, and PSY accumulation).</p><p>Our findings demonstrate that RAPA significantly enhances motor functions at specific treatment time points and reduces astrogliosis in TWI brain, spinal cord, and sciatic nerves. Using western blot and immunohistochemistry, we observed a decrease in p62 aggregates in TWI nervous tissues, which corroborates our earlier in-vitro results. Furthermore, RAPA treatment partially reduces PSY levels in the spinal cord.</p><p>In conclusion, our results support the consideration of RAPA as a supportive therapy for KD. Importantly, as RAPA is already available in pharmaceutical formulations for clinical use, its potential for KD treatment can be promptly evaluated in clinical trials.</p>
Single-cell transcriptomic profiling unveils dysregulation of cardiac progenitor cells and cardiomyocytes in a mouse model of maternal hyperglycemia
<p>Congenital heart disease (CHD) is the most prevalent structural malformations of the heart affecting ∼1% of live births. To date, both damaging genetic variations and adverse environmental exposure such as maternal diabetes have been found to cause CHD. Clinical studies show ∼fivefold higher risk of CHD in the offspring of mothers with pregestational diabetes. Maternal pregestational diabetes affects the gene regulatory networks key to proper cardiac development in the fetus. However, the cell-type specificity of these gene regulatory responses to maternal diabetes and their association with the observed cardiac defects in the fetuses remains unknown. To uncover the transcriptional responses to maternal diabetes in the early embryonic heart, we used an established murine model of pregestational diabetes. In this model, we have previously demonstrated an increased incidence of CHD. Here, we show maternal hyperglycemia (matHG) elicits diverse cellular responses during heart development by single-cell RNA-sequencing in embryonic hearts exposed to control and matHG environment. Through differential gene-expression and pseudotime trajectory analyses of this data, we identified changes in lineage specifying transcription factors, predominantly affecting Isl1+ second heart field progenitors and Tnnt2+cardiomyocytes with matHG. Using in vivo cell-lineage tracing studies, we confirmed that matHG exposure leads to impaired second heart field-derived cardiomyocyte differentiation. Finally, this work identifies matHG-mediated transcriptional determinants in cardiac cell lineages elevate CHD risk and show perturbations in Isl1-dependent gene-regulatory network (Isl1-GRN) affect cardiomyocyte differentiation. Functional analysis of this GRN in cardiac progenitor cells will provide further mechanistic insights into matHG-induced severity of CHD associated with diabetic pregnancies.</p>
Peripheral MC1R activation modulates immune responses and confers neuroprotection in a mouse model of Parkinson's disease
<p>Raw data sets for the manuscripts</p> <p>This work was supported by NIH grants R01NS102735 and R01NS110879, the Farmer Family Foundation Initiative for Parkinson’s Disease Research and the MJFF and ASAP [ASAP-000312].</p>
Connectomes, APOE, Age, Sex, and Diet in Mouse Models of Aging
<p>Brain networks and covariates for mouse models of aging. Includes APOE22/33/44 with and without HN, age, sex, and diet.</p> <p>Files:</p> <p>- connectomes.rda: a tensor of symmetric adjacency matrices corresponding to brain networks.</p> <p>- mice.rda: a dataframe containing mouse covariates.</p> <p>- mouse_anatomy.csv: a table containing scientific names for each brain region in connectomes.rda.</p>
Structure of the Nt domain of mouse NBCe1 by homology modeling
<p>For the generation of the Nt model for NBCe1, a pair-wise alignment of the Nt region (residues 82-381) of mouse NBCe1-B (NCBI accession NP_061230.2) and the homologous portion of human NDCBE Nt (NCBI accession AAY79176) was generated by SWISS-MODEL. The overall identity is 54.55% between the two sequences. The alignment was used for structural modeling with the crystal structure of human NDCBE Nt (PDB ID: 5JHO) as the template. Structural assessment shows that the simulated model of NBCe1 Nt had QMEAN value −3.25, Cβ value −3.11, solvation value −0.62, torsion value −2.54, and scored 1.86 by using a MolProbity approach.</p>
Biochemical Characterization of Mouse Retina of an Alzheimer's Disease Model by Raman Spectroscopy
<p>Raman raw data for the paper "Biochemical Characterization of Mouse Retina of an Alzheimer’s Disease Model by Raman Spectroscopy"</p> <ul> <li>two datasets of Raman images from cross-sectional and en face mouse retinas without processing</li> </ul>
Raw dataset and additional data for article "Nonmotor symptoms associated with progressive loss of dopaminergic neurons in a mouse model of Parkinson's disease"
<p>Dataset from the project investigating the presence of nonmotor symptoms of Parkinson's disease in a mouse model of progressive loss of dopaminergic neurons (namely,TIF-IADATCreERT2 strain). Mice were tested for executive and cognitive functions (males: Operant Sensation Seeking test, OSS; females: Probabilistic Reversal Learning Task in Intellicages), olfactory acuity (males: buried food test), saccharin preference (males and females), and motor performance (males and females: test using CatWalk apparatus).</p><p>The dataset includes files used to perform statistical analyses but their names may vary from the ones used in the scripts. For the purpose of recreating our analyses, please refer to the GitHub page, where both scripts and input data file names (in 'Raw data files' section) are compliant: https://github.com/annaradli/tif-pd-behavior.</p><p><strong>Description of files:</strong></p><p><i>Raw data files:</i></p><ul><li>animals_info.csv - animals data: genotype, sex, age, Intellicage tag identifier</li><li>catwalk_run_statistics_all_females.csv - data recorded in CatWalk apparatus for females</li><li>catwalk_run_statistics_all_males.csv - data recorded in CatWalk apparatus for males</li><li>females_weight_raw_data_revised.csv - females' body weight (revised for containing Polish words)</li><li>intellicage_raw_data.csv - data recorded in IntelliCage exported to .csv format</li><li>intellicage_raw_data_R.RData - data recorded in IntelliCage in .RData format</li><li>males_weight_raw_data.csv - males' body weight</li><li>olfactory_time_digging_raw_data.csv - time to start digging at the right place in the buried food test</li><li>olfactory_time_retrieve_raw_data.csv- time to retrieve cracker in the buried food test</li><li>oss_raw_data.csv - data recorded in the OSS test</li><li>saccharin_preference_males_raw_data.csv - saccharin preference test results for males</li><li>snvta_cells_count.csv - number of TH+ cells in SN and VTA in male mice (3+3) 14 weeks after tamoxifen treatment</li></ul><p><i>Additional data files:</i></p><ul><li>all_anova.xlsx - summary of two-way ANOVAs of all behavioral tests and weight measurements for males and females</li><li>catwalk_complete.xlsx - CatWalk complete dataset with datapoints</li><li>catwalk_correlation_between_paws.xlsx - correlation coefficients of CatWalk parameters between the left and right paws</li><li>catwalk_reduced.xlsx - CatWalk parameters used in linear regression model reduction of data</li><li>intelli.xlsx - IntelliCage data summarized in bins</li><li>oss.xlsx - operant sensation-seeking data</li></ul><p>v2 contains the corrected 'animals_info.csv' file without an unnecessary column.</p><p>v3 has a revised version of file containing females' weight measurements and also added a file with midbrain cell counts</p><p>v4 has a whole section of 'Additional data files' added</p>
Dataset Friebus-Kardash et al, A chemerin peptide analog stimulates tumor growth in two xenograft mouse models of human colorectal carcinoma
<p>Dataset Friebus-Kardash et al, A chemerin peptide analog stimulates tumor growth in two xenograft mouse models of human colorectal carcinoma</p> <p> </p>
Fig. 5. The marginal response curve for the explanatory variable Bio14 in Modelling The Bioclimatic Niche And Distribution Of The Steppe Mouse, Mus Spicilegus (Rodentia, Muridae), In Ukraine
Fig. 5. The marginal response curve for the explanatory variable Bio14 (Precipitation of driest week). (HS — habitat suitability).
Fig. 1 in Modelling The Bioclimatic Niche And Distribution Of The Steppe Mouse, Mus Spicilegus (Rodentia, Muridae), In Ukraine
Fig. 1. Occurrences of Mus spicilegus in Ukraine and neighbouring areas used for creating the ENM. [Data collected before (triangles) and after (circles) 1990.]
Fig. 4. The marginal response curve for the explanatory variable Bio09 in Modelling The Bioclimatic Niche And Distribution Of The Steppe Mouse, Mus Spicilegus (Rodentia, Muridae), In Ukraine
Fig. 4. The marginal response curve for the explanatory variable Bio09 (Mean temperature of driest quarter). (HS — habitat suitability).
Fig. 7. 0.5 in Modelling The Bioclimatic Niche And Distribution Of The Steppe Mouse, Mus Spicilegus (Rodentia, Muridae), In Ukraine
Fig. 7. 0.5 oC isotherms for Bio09 (Mean temperature of driest quarter) for different time periods: 1 — 1980s; 2 — 2000s; 3 — contemporary; 4 — predicted for 2030.
Fig. 6. A in Modelling The Bioclimatic Niche And Distribution Of The Steppe Mouse, Mus Spicilegus (Rodentia, Muridae), In Ukraine
Fig. 6. A current climate habitat suitability map for the Steppe mouse (Mus spicilegus) in Ukraine. Darker shades of gray denote areas of higher predicted habitat suitability probabilities (≥ 0.5) and lighter shades correspond to lower (≥ 0.311 and <0.5). [Administrative regions in Ukraine: 1 — Chernihiv Region; 2 — Kyiv Region; 3 — Ternopil Region; 4 — Ivano-Frankivsk Region.]
Gene drives for vertebrate pest control: realistic spatial modelling of eradication probabilities and times for island mouse populations
<p>Invasive alien species continue to threaten global biodiversity. CRISPR-based gene drives, which can theoretically spread through populations despite imparting a fitness cost, could be used to suppress or eradicate pest populations. We develop an individual-based, spatially explicit, stochastic model to simulate the ability of CRISPR-based homing and X-chromosome shredding drives to eradicate populations of invasive mice (Mus muculus) from islands. Using the model, we explore the interactive effect of the efficiency of the drive constructs and the spatial ecology of the target population on the outcome of a gene-drive release. We also consider the impact of polyandrous mating and sperm competition, which could compromise the efficacy of some gene-drive strategies. Our results show that both drive strategies could be used to eradicate large populations of mice. Whereas parameters related to drive efficiency and demography strongly influence drive performance, we find that sperm competition following polyandrous mating is unlikely to impact the outcome of an eradication effort substantially. Assumptions regarding the spatial ecology of mice influenced the probability of and time required for eradication, with short-range dispersal capabilities and limited mate-search areas producing `chase' dynamics across the island characterised by cycles of local extinction and recolonization by mice. We also show that highly efficient drives are not always optimal, when dispersal capabilities are low, rapid local population supression around the introduction sites can cause loss of the gene drive before it can spread to the entire island. We conclude that, although the design of efficient gene drives is undoubtedly critical, accurate data on the spatial ecology of target species is critical for predicting the result of a gene-drive release.</p>
MyD88-TLR4-dependent choroid plexus activation precedes perilesional inflammation and secondary brain edema in a mouse model of intracerebral hemorrhage
<p>Supplementary data and code of the article "MyD88-TLR4-dependent choroid plexus activation precedes perilesional inflammation and secondary brain edema in a mouse model of intracerebral hemorrhage".</p>
Pre-processed ex vivo MRI data for manuscript titled "Neuroanatomical and cognitive biomarkers of alpha-synuclein propagation in a mouse model of synucleinopathy prior to onset of motor symptoms""
<p>Repository for <em>ex vivo</em> magnetic resonance imaging data from the project titled "Presymptomatic neuroanatomical and cognitive biomarkers of alpha-synuclein propagation in a mouse model of synucleinopathy"</p> <p>Contains the pre-processed <em>ex vivo</em> T1-weighted images (Bruker 7T; 70 micron isotropic voxel resolution) for M83 alpha-synuclein A53T hemizygous mice that received either a phosphate buffered saline (PBS) or alpha-synuclein pre-formed fibrils (PFF) injection in the right dorsal striatum. Full subject list can be viewed with the "subject_list.csv" file. More details are available in the manuscript. </p>
Electrophysiological data of the paper 'Serotonergic and dopaminergic neurons in the dorsal raphe are differentially altered in a mouse model for parkinsonism'
<p>This excel data set contains the electrophysiological data presented in the paper including figure 1I, 1J, figure 3, figure 5, suppl. figure 2A, suppl. figure 3, suppl. figure 6E, 6G, 6L & 6N.</p> <p> </p> <p>More information about how the data was extracted can be found in the materials and methods section of the paper. </p>
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.