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2,709 results for “mouse models”
Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction
<p>The raw data of the manuscript” Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction”</p>
PINK1 deficiency rewires early immune responses in a mouse model of Parkinson's disease triggered by intestinal infection
<p>Parkinson’s disease is characterized by a period of non-motor symptoms, including gastrointestinal dysfunction, preceding motor deficits by decades. This long prodrome is suggestive of peripheral immunity involvement in the initiation of disease. We previously developed a model system in PINK1 KO mice displaying PD-like motor symptoms at late stages following intestinal infections. Herein, we map the initiating immune events at the site of infection in this model. Using single-cell RNAseq, we demonstrate that peripheral myeloid cells are the earliest highly dysregulated immune cell type in PINK1 KO infected mice followed by an aberrant T cell response shortly after. We elucidate an increased propensity for antigen presentation mediated by myeloid-CD8+ T cell interaction. PINK1 KO activated myeloid cells acquire a proinflammatory profile inducing cytotoxic T cell responses. Together, our study provides the first evidence that PINK1 is a key regulator of immune functions in the gut underlying early PD-related disease mechanisms.</p>
Data from: Effect of stretching on inflammation in a subcutaneous carrageenan mouse model analyzed at single-cell resolution
<p>Understanding the factors that influence the biological response to inflammation is crucial, due to its involvement in physiological and pathological processes, including tissue repair/healing, cancer, infections, and autoimmune diseases. We have previously demonstrated that in vivo stretching can reduce inflammation and increase local pro-resolving lipid mediators in rats, suggesting a direct mechanical effect on inflammation resolution. Here, we aimed to explore further the effects of stretching at the cellular/molecular level in a mouse subcutaneous carrageenan-inflammation model. Stretching for 10 minutes twice a day reduced inflammation, increased the production of pro-resolving mediator pathway intermediate 17-HDHA at 48h post carrageenan injection, and decreased both pro-resolving and pro-inflammatory mediators (e.g., PGE<sub>2</sub> and PGD<sub>2</sub>) at 96h. ScRNAseq analysis of inflammatory lesions at 96h showed that stretching increased the expression of both pro-inflammatory (<em>Nos2</em>) and pro-resolution (<em>Arg1</em>) genes in M1 and M2 macrophages at 96 hours. An intercellular communication analysis predicted specific ligand-receptor interactions orchestrated by neutrophils and M2a macrophages, suggesting a continuous neutrophil presence recruiting immune cells such as activated macrophages to contain the antigen while promoting resolution and preserving tissue homeostasis.</p>
Feature attention graph neural network for estimating brain age and identifying important neural connections in mouse models of genetic risk for Alzheimer's disease
<p>Connectome, traits and behavior data for APOE234 mice.</p> <ul> <li>1. connectome.zip: mouse brain structural connectivity matrices from diffusion MRI.</li> <li>2. FAGNN_Phenotype.csv: a sheet of trait information of mice used in the study.</li> </ul> <p>columns: winding numbers, total distance, normalized NE time, normalized NE distance, normalized NW time, normalized NW distance, normalized SE time, normalized SE distance, normlaized SW time, normalized SW distance, island latency to first entry, island entries, normalized thigmataxis time, and normalized thigmotaxis distance</p> <div>rows: 4 trials for each day from day 1 to day 5 with 1 probing test each at day 5 and day 8</div> <ul> <li>3. mouse_anatomy.csv: brain region information regarding the connectivity matrix.</li> <li>4. behavior.zip: behavioral data for each mouse from Morris Water Maze experiments.</li> </ul>
Data from: Metabolomic profiles of acute and chronic ambient hydrogen sulfide exposure in a mouse model
<p>Hydrogen sulfide (H<sub>2</sub>S) is an environmental toxicant of health concern following acute or chronic human exposures. Male 6-8 week-old C57BL/6J mice were exposed by whole-body inhalation to 1000 ppm H<sub>2</sub>S for 45 min and euthanized at 5 min and 72 h for acute exposure. For subchronic study, mice were exposed to 5 ppm H<sub>2</sub>S 2 h/day, 5 days/week for 5 weeks. The brainstem was removed for metabolomic analysis. The metabolomics analyses consisted of three assays, (1) primary metabolism by GC-TOF MS, (2) biogenic amines (hydrophilic compounds) by HILIC-MS/MS and (3) lipidomics by RPLC-MS/MS. Metabolomics were performed in West Coast Metabolomics Center, University of California at Davis, CA, USA. 348, 311, and 565 known metabolites were detected and analyzed by primary metabolism, biogenic amines, and lipidomic metabolomics assays. 33, 19, and 46 metabolites were increased at 5 min and 72 h post acute H<sub>2</sub>S exposures and subchronic ambient H<sub>2</sub>S exposures, respectively, compared to room air control group. 22, 17, and 32 metabolites were decreased at 5 min and 72 h post acute H<sub>2</sub>S exposures and subchronic ambient H<sub>2</sub>S exposures, respectively, compared to room air control group. Acute H<sub>2</sub>S exposure decreased excitatory neurotransmitters aspartate and glutamate concentrations while the inhibitory neurotransmitter serotonin was increased. Glutamate and serotonin were also decreased after ambient H<sub>2</sub>S exposure. Branched-chain amino acids, fructose, and glucose were increased by acute H<sub>2</sub>S exposure. In ambient H<sub>2</sub>S exposure, glucose was decreased while MUFAs, PUFAs, inosine, and hypoxanthine were increased. Collectively, these results provide important mechanistic clues of acute and subchronic ambient H<sub>2</sub>S poisonings and show that H<sub>2</sub>S alters neurotransmission homeostasis.</p>
mRNA prime–boost evolves precursors toward VRC01-like broadly neutralizing antibodies in preclinical humanized mouse models
<p>Germline-targeting (GT) protein immunogens to induce VRC01-class broadly neutralizing antibodies (bnAbs) to the CD4 binding site (CD4bs) of the HIV Envelope have shown promise in clinical trials. Here, we preclinically validated the mRNA-LNP delivery of one such immunogen, eOD-GT8, as a soluble self-assembling 60mer nanoparticle in humanized mouse models. In a model with three humanized B cell lineages bearing distinct VRC01-precursor B cell receptors (BCRs) with similar affinities for eOD-GT8, all lineages could be simultaneously primed and undergo diversification and affinity maturation with no sign of exclusionary competition. Boosts drove precursor B cell participation in germinal centers, the accumulation of somatic hypermutations, including in key VRC01-class positions, and affinity maturation to boost and native-like antigens in two of the three precursor lineages. We have preclinically validated a prime-boost regimen of soluble self-assembling nanoparticles delivered by mRNA-LNP, demonstrating that multiple lineages can be primed, boosted, and diversify along the bnAb pathway.</p>
Inhibition of DKK-1 Limits Osteosarcoma Metastasis in a Clinically Relevant Mouse Model
<p>Single-cell RNA-seq data of untreated (F43N, F43R) and DKK-1 inhibitor treated (OSW3, OSW4, OSW5, OSW6) patient derived xenografts (PDXs). </p> <p>human_cells_scanpy_object.h5ad -- contains Scanpy analysis of human cells from untreated and DKK-1 inhibitor treated PDXs</p> <p>raw_counts_cellranger_output.zip -- contains the raw expression counts of untreated and DKK-1 inhibitor treated PDXs cells outputted by CellRanger. </p>
Metadata - A New Application for Cenicriviroc, a Dual CCR2/CCR5 Antagonist, in the Treatment of Painful Diabetic Neuropathy in a Mouse Model
Open the record for dataset details and reuse information.
Hematopoietic Tumors in a Mouse Model of X-linked Chronic Granulomatous Disease after Lentiviral Vector-Mediated Gene Therapy
<p>Chronic granulomatous disease (CGD) is a rare inherited disorder due to loss-of-function mutations in genes encoding the NADPH oxidase subunits. Hematopoietic stem and progenitor cell (HSPC) gene therapy (GT) using regulated lentiviral vectors (LVs) has emerged as a promising therapeutic option for CGD patients. We performed non-clinical Good Laboratory Practice (GLP) and laboratory-grade studies to assess the safety and genotoxicity of LV targeting myeloid specific Gp91phox expression in X-linked chronic granulomatous disease (XCGD) mice. We found persistence of gene-corrected cells for up to 1 year, restoration of Gp91phox expression and NADPH oxidase activity in XCGD phagocytes, and reduced tissue inflammation after LV-mediated HSPC GT.<br> Although most of the mice showed no hematological or biochemical toxicity, a small subset of XCGD GT mice developed<br> T cell lymphoblastic lymphoma (2.94%) and myeloid leukemia (5.88%). No hematological malignancies were identified in C57BL/6 mice transplanted with transduced XCGD HSPCs. Integration pattern analysis revealed an oligoclonal composition with rare dominant clones harboring vector insertions near oncogenes in mice with tumors. Collectively, our data support the long-term efficacy of LV-mediated HSPC GT in XCGD mice and provide a safety warning because the chronic inflammatory XCGD background may contribute to oncogenesis.</p>
Modelling the genetic aetiology of complex disease: human-mouse conservation of noncoding features and disease-associated loci
<p>Understanding the genetic aetiology of loci associated with disease is crucial for developing preventative measures and effective treatments. Mouse models are used extensively to understand human pathobiology and mechanistic functions of disease-associated loci. However, the utility of mouse models is limited by evolutionary divergence in transcription regulation for pathways of interest. Here, we summarise the conservation of genomic (exonic and multi-cell regulatory) features and complex disease associated variant sites between humans and mice. Our results highlight the importance of understanding evolutionary divergence in transcription regulation when interpreting functional studies using mice as models for human disease variants.</p>
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
<p class="MsoNormal">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/<em>Usp16<sup><span>+/-</span></sup></em> NPCs, respectively, we performed single-cell RNA-seq and gene set enrichment analysis (GSEA) on lineage depleted primary FACS-sorted CD31<sup><span>-</span></sup>CD45<sup><span>-</span></sup>Ter119<sup><span>-</span></sup>CD24<sup><span>-</span></sup> NPCs from Tg-SwDI, WT, and Tg-SwDI/<em>Usp16<sup><span>+/-</span></sup></em> 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/<em>Usp16<sup><span>+/-</span></sup> </em>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/<em>Usp16<sup><span>+/-</span></sup> </em>of the three rescued pathways. These data suggest that USP16 may regulate neural precursor cell function in part through the BMP pathway.</p>
In vivo characterization of antibodies directed against TREAT-AD target proteins in mouse model of AD pathology
<p><em>In vivo </em>characterization of antibodies directed against TREAT-AD target proteins (Moesin, CD44, Midkine, and SFRP1) in the 5xFAD mouse model</p>
Systemic application of the TRPV4 antagonist GSK2193874 induces tail vasodilation in a mouse model of thermoregulation
<p>In humans, skin is a primary thermoregulatory organ, with vasodilation leading to rapid body cooling, whereas in Rodentia the tail performs an analogous function. Many thermodetection mechanisms are likely to be involved including transient receptor potential vanilloid-type 4 (TRPV4), an ion channel with thermosensitive properties. Previous studies have shown that TRPV4 is a vasodilator by local action in blood vessels, so here we investigated whether constitutive TRPV4 activity effects <em>Mus muscularis</em> tail vascular tone and thermoregulation. We measured tail blood flow by pressure plethysmography in lightly sedated Mus muscularis (CD1 strain) at a range of ambient temperatures, with and without intraperitoneal administration of the blood brain barrier crossing TRPV4 antagonist GSK2193874. We also measured heart rate and blood pressure. As expected for a thermoregulatory organ, we found that tail blood flow increased with temperature. However, unexpectedly we found that GSK2193874 increased tail blood flow at all temperatures, and we observed changes in heart rate variability. Since local TRPV4 activation causes vasodilation that would increase tail blood-flow, these data suggest that increases in tail blood flow resulting from the TRPV4 antagonist may arise from a site other than the blood vessels themselves, perhaps in central cardiovascular control centres.</p>
MALDI-MS raw files of primary human lung cancer samples, lung cancer patient derived xenografts and lung cancer mouse models
<p>Human primary lung cancer samples, patient derived lung cancer xenografts and lung tumors from the TetO-KRASG12D mouse model were analyzed using MALDI-MS. We determined the spatial distribution and relative abundance of lipids of interest. </p>
Rapid and specific degradation of endogenous proteins in mouse models using auxin-inducible degrons
<p>Auxin-inducible degrons are a chemical genetic tool for targeted protein degradation and are widely used to study protein function in cultured mammalian cells. Here we develop CRISPR-engineered mouse lines that enable rapid and highly specific degradation of tagged endogenous proteins <em>in vivo</em>. Most but not all cell types are competent for degradation. By combining ligand titrations with genetic crosses to generate animals with different allelic combinations, we show that degradation kinetics depend upon the dose of the tagged protein, ligand, and the E3 ligase substrate receptor TIR1. Rapid degradation of condensin I and condensin II – two essential regulators of mitotic chromosome structure - revealed that both complexes are individually required for cell division in precursor lymphocytes, but not in their differentiated peripheral lymphocyte derivatives. This generalisable approach provides unprecedented temporal control over the dose of endogenous proteins in mouse models, with implications for studying essential biological pathways and modeling drug activity in mammalian tissues.</p>
Source Data files for: Primary cilia and SHH signaling impairments in human and mouse models of Parkinson's disease
<p>Parkinson’s disease (PD) as a progressive neurodegenerative disorder arises from multiple genetic and environmental factors. However, underlying pathological mechanisms remain poorly understood. Using multiplexed single-cell transcriptomics, we analyze human neural precursor cells (hNPCs) from sporadic PD (sPD) patients. Alterations in gene expression appear in pathways related to primary cilia (PC). Accordingly, in these hiPSC-derived hNPCs and neurons, we observe a shortening of PC. Additionally, we detect a shortening of PC in <em>PINK1</em>-deficient human cellular and mouse models of familial PD. Furthermore, in sPD models, the shortening of PC is accompanied by an increased SHH signal transduction. Inhibition of this pathway rescues the alterations in PC morphology and mitochondrial dysfunction. Thus, increased SHH activity due to ciliary dysfunction is needed for the development of pathoetiological phenotypes observed in sPD, like mitochondrial dysfunction. In sum, altered PC function is part of early PD pathoetiology and inhibiting the overactive SHH signaling is a potential neuroprotective therapy.</p>
Machine learning on syngeneic mouse tumor profiles to model clinical immunotherapy response
<p><span>Most cancer patients are refractory to immune checkpoint blockade (ICB) therapy, and proper patient stratification remains an open question. Primary patient data suffer from high heterogeneity, low accessibility, and lack of proper controls. In contrast, syngeneic mouse tumor models enable controlled experiments with ICB treatments. Using transcriptomic and experimental variables from >700 ICB-treated/control syngeneic mouse tumors, we developed a novel machine learning framework to model tumor immunity and identify factors influencing ICB response. Projected on human immunotherapy trial data, we found that the model can predict clinical ICB response. We further applied the model to predicting ICB-responsive/resistant cancer types in TCGA, which agreed well with existing clinical reports. Finally, feature analysis implicated factors associated with ICB response. In summary, our novel computational framework based on mouse tumor data reliably stratified patients regarding ICB response, informed resistance mechanisms, and has the potential for wide applications in disease treatment studies.</span></p>
Imbalanced expression of cation-chloride cotransporters as a potential therapeutic target in an Angelman Syndrome mouse model
<p>We provide 6 files; 1. Data for western blot analysis (WB_NKCC1_KCC2_Fig1A.xlsx), 2. Data for [Cl-]i(Intracelluar‗Cl_Fig1B.xlsx), 3. Electrophysilogical data for mIPSC and tonic current (mIPSC_Tonic current_Fig2B_C_E.xlsx), 4. Data for behavior analysis (Behavior_analysis_Fig3A_C .xlsx), 5. Data for seizure threshhold (seizure_threshold_Fig4A.xlsx), 6. Data for EEG spike number and band power (EEG_analysis_Fig4B_C.xlsx)</p>
Gene augmentation prevents retinal degeneration in a CRISPR/Cas9-based mouse model of PRPF31 retinitis pigmentosa
<p>Mutations in <em>PRPF31</em> cause autosomal dominant retinitis pigmentosa, an untreatable form of blindness. Gene therapy is a promising treatment for <em>PRPF31</em>-retinitis pigmentosa, however, there are currently no suitable animal models in which to develop AAV-mediated gene augmentation. Here we establish <em>Prpf31</em> mutant mouse models using AAV-mediated CRISPR/Cas9 knockout, and characterize the resulting retinal degeneration phenotype. Mouse models with early-onset morphological and functional impairments like those in patients were established, providing new platforms in which to investigate pathogenetic mechanisms and develop therapeutic methods. AAV-mediated <em>PRPF31</em> gene augmentation restored the retinal structure and function in a rapidly degenerating mouse model, demonstrating the first in vivo proof-of-concept for AAV-mediated gene therapy to treat <em>PRPF31</em>-retinitis pigmentosa. AAV-CRISPR/Cas9-PRPF31 knockout constructs also mediated efficient <em>PRPF31</em> knockout in human and non-human primate retinal explants, laying a foundation for establishing non-human primate models using the method developed here.</p>
Additional raw video and pose estimation data of top view mouse behavior recordings (marble burying test, light-dark box, fear conditioning box) of acute and chronic stress models
<p>This repository contains raw data for 296 different behavioral recordings of mice (marble burying test, light-dark box, fear conditioning box). These include top view raw video .mp4 files (Videos.zip) and the corresponding .csv pose estimation data (data.zip) obtained with DeepLabCut. The data is from multiple different experiments. The METADATA.csv or METADATA.xlsx files contain all grouping variables and help linking the pose estimation files (located in multiple subfolders of /data) to the video files. Visit https://github.com/ETHZ-INS/BehaviorFlow to find out more about how this data has be used by us.</p>
ScienceDex guides
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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.