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2,709 results for “mouse models”
Spatial transcriptomics of an innate granuloma in a mouse infection model with Chromobacterium violaceum
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Data from: A nanovaccine for immune activation and prophylactic protection of atherosclerosis in mouse models
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Dietary ketosis improves circadian dysfunction as well as motor symptoms in the BACHD mouse model of Huntington’s disease
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The impact of Rhodiola Rosea on biomarkers of diabetes, inflammation, and microbiota in a leptin receptor-knockout mouse model
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Data from: Development of an adrenocortical cancer humanized mouse model to characterize anti-PD1 effects on tumor microenvironment
Context: While the development of immune checkpoint inhibitors has transformed treatment strategies of several human malignancies, research models to study immunotherapy in ACC are lacking. Objective: To explore the effect of anti-PD1 immunotherapy on the alteration of the immune milieu in ACC in a newly generated preclinical model and correlate with the response of the matched patient. Design, Setting and Intervention: To characterize the CU-ACC2-M2B patient-derived xenograft in a humanized mouse model, evaluate the effect of a PD-1 inhibitor therapy and compare to the CU-ACC2 patient with metastatic disease. Results: Characterization of the CU-ACC2-hu-CB-BRGS model confirmed ACC origin and match with the original human tumor. Treatment of the mice with pembrolizumab demonstrated significant tumor growth inhibition (TGI = 60%) compared to controls, which correlated with increased tumor infiltrating lymphocyte activity, with an increase of human CD8+ T cells (p<0.05), HLA-DR+ T cells (p<0.05) as well as Granzyme B+ CD8+ T cells (<0.001). In parallel, treatment of the CU-ACC2 patient, who had progressive disease, demonstrated a partial response with 79%-100% reduction in the size of target lesions, and no new sites of metastasis. Pre-treatment analysis of the patient's metastatic liver lesion demonstrated abundant intra-tumoral CD8+ T cells by immunohistochemistry. Conclusions: Our study reports the first humanized ACC PDX mouse model which may be useful to define mechanisms and biomarkers of response and resistance to immune-based therapies, to ultimately provide more personalized care for patients with ACC.
Structure of transmembrane domain of mouse NBCe1 by homology modeling
<p>The structure model of the transmembrane domain of mouse NBCe1 was generated by SWISS-MODEL with the cryo-EM structure of human NBCe1 (PDB ID: 6CAA) as the template. Residues 445–1007 of mouse NBCe1-B was aligned with the homologous region of human NBCe1 by using SWISS-MODEL. The sequence identity between the two sequences is 96.09%. Structural assessment shows that the simulated model of mouse NBCe1 had QMEAN value −6.86, Cβ −3.57, solvation value −1.80, torsion value −5.49, and scored 1.49 by MolProbity approach.</p>
Decreased content of ascorbic acid (vitamin C) in the brain of knockout mouse models of Na+, K+- ATPase-related neurologic disorders
<p><strong><span><span><span><span><span><span><span><span><span><span><span>Raw data, a2Ca3-dKO phenotype and dystonic spell of a3-HT</span></span></span></span></span></span></span></span></span></span></span></strong></p> <p><strong><span><span><span><span><span><span><span><span><span><span><span>We found brain haemorrhage phenotype of Atp1a2 and Atp1a3 doule knockout (α2α3-dKO) foetuses. Here we present two kinds of α2α3-dKO line, α2-Nα3-dKO andα2-Cα3-dKO, both show brain haemorrhage upon birth. They were similar to that of homozygous knockout of the gene encoding ascorbic acid (ASC orNvitamin C) transporter, SVCT2 (SVCT2-KO). We made SVCT2-knockout mouse line by CRIPR/CAS9 method. We present SVCT2-KO, showing brain hemorrage as α2α3-dKO. The α2α3-dKO and SVCT2-KO brain showed significantly decreased level of ASC compared with the wild-type (WT) and single knockout (here, raw data). We found that the ASC content in the basal ganglia and cerebellum was significantly lower in the adult <i>Atp1a3 </i>heterozygous knockout mouse (α3-HT) than in the WT (here, raw data). We did not observe increased oxidative stress in them (here raw data). Interestingly, we observed a significant decrease in the ASC level in the basal ganglia and cerebellum of α3-HTin the peripartum period, during which mice are under physiological stress(here, raw data). Here, we show dystonic spell of α3-HT in peripartum. These observations indicate that the α2 and α3 subunits independently contribute to the ASC level in the foetal brain and that the α3 subunit contributes to ASC transport in the adult basal ganglia and cerebellum. We propose that decreases in ASC levels may affect neural network development and are linked to the pathophysiology of <i>ATP1A2- </i>and <i>ATP1A3</i>-related neurologic disorders.</span></span></span></span></span></span></span></span></span></span></span></strong></p>
Proteinuric chronic kidney disease mouse model RNAseq
<p>RNA seq in renal cortex from proteinuric CKD mouse model</p>
Data from: Nanotransfection-based vasculogenic cell reprogramming drives functional recovery in a mouse model of ischemic stroke
<p>Ischemic stroke causes vascular and neuronal tissue deficiencies that could lead to significant functional impairment and/or death. Although progenitor-based vasculogenic cell therapies have shown promise as a potential rescue strategy following ischemic stroke, current approaches face major hurdles. Here we used fibroblasts nanotransfected with <em>Etv2</em>, <em>Foxc2</em>, and <em>Fli1</em> (<em>EFF</em>), to drive reprogramming-based vasculogenesis, intracranially, as a potential therapy for ischemic stroke. Perfusion analyses suggest that intracranial delivery of <em>EFF</em>-nanotransfected fibroblasts led to a dose-dependent increase in perfusion 14 days post-injection. MRI and behavioral tests revealed ~70% infarct resolution and up to ~90% motor recovery for mice treated with <em>EFF</em>-nanotransfected fibroblasts. Immunohistological analysis confirmed increases in vascularity and neuronal cellularity, as well as reduced glial scar formation in response to treatment with <em>EFF</em>-nanotransfected fibroblasts. Altogether, our results suggest that vasculogenic cell therapies based on nanotransfection-driven (i.e., non-viral) cellular reprogramming represent a promising strategy for the treatment of ischemic stroke.</p>
03/04 - Spatial and Amplitude Dynamics of Neurostimulation: Insights from the Acute Intrahippocampal Kainate Seizure Mouse Model
<p>Dataset #3 of 4</p>
01/04 - Spatial and Amplitude Dynamics of Neurostimulation: Insights from the Acute Intrahippocampal Kainate Seizure Mouse Model
<p>Dataset #1 of 4</p>
Reproducible network changes occur in a mouse model of temporal lobe epilepsy but do not correlate with disease severity
<p><strong>Dataset for the publication: 'Reproducible network changes occur in a mouse model of temporal lobe epilepsy but do not correlate with disease severity '</strong><br><strong>Rigoni et al. 2023, Neurobiology of Disease, doi: <a title="Persistent link using digital object identifier" href="https://doi.org/10.1016/j.nbd.2023.106382" target="_blank" rel="noreferrer noopener"><span>https://doi.org/10.1016/j.nbd.2023.106382</span></a></strong></p> <p><strong>Dataset description</strong></p> <p><em>Data\data2publish\sub- </em>: 50 epochs of raw epicranial EEG data (31 x 8001 x 50, channels x time x n_epochs,<em> </em>Fs=4k Hz). The epochs are available for 29 mice, on different sessions (ses-d0, ses-d28, ses-d29) depending on the animal </p> <p><em>Data\data2publish\EA_info.xlsx</em>: number of epileptiform activities automatically detected for each animal at d28 and d29</p> <p><em>Data\data2publish\derivatives\eeg_preprocessing: </em>results of the script A_EEG_preprocessing.m, for each animal and session</p> <p><em>Data\data2publish\derivatives\elec_layout: </em>different layouts used to plot results. Mouse_layout_modif is the one used in Fig 4</p> <p><em>Data\data2publish\derivatives\network_metrics</em>_<em>wpli: </em>results of network analyses (script C_network_analyses.m)</p> <p><em>Data\data2publish\derivatives\wpli</em>: connectivity matrices (30 x 30) obtained with the script B_connectivity_wpli.m for each animal, in each session, for each frequency band wit</p> <p><strong>Code for analyses available here: </strong> <a href="https://github.com/IsottaR/ir_mice_project_Zenodo">https://github.com/IsottaR/ir_mice_project_Zenodo </a></p> <p>Abbreviations:</p> <p>EEG= electroencephalography</p>
JNK Activation Correlates with Cognitive Impairment and Alteration of the Post-Synaptic Element in the 5xFAD AD Mouse Model
<p>The c-Jun N-terminal kinases (JNKs) are a family of proteins that, once activated by stress<br>stimuli, can alter neuronal functions and survival. The JNK cascade plays a crucial role in the<br>post-synaptic neuronal compartment by altering its structural organization and leading, at worst,<br>to an overall impairment of neuronal communication. Increasing evidence suggests that synaptic<br>impairment is the first neurodegenerative event in Alzheimer’s disease (AD). To better elucidate this<br>mechanism, we longitudinally studied 5xFAD mice at three selected time points representative of<br>human AD symptom progression. We tested the mice cognitive performance by using the radial<br>arm water maze (RAWM) in parallel with biochemical evaluations of post-synaptic enriched protein<br>fraction and total cortical parenchyma. We found that 5xFAD mice presented a strong JNK activation<br>at 3.5 months of age in the post-synaptic enriched protein fraction. This JNK activation correlates<br>with a structural alteration of the post-synaptic density area and with memory impairment at this<br>early stage of the disease that progressively declines to cause cell death. These findings pave the way<br>for future studies on JNK as a key player in early neurodegeneration and as an important therapeutic<br>target for the development of new compounds able to tackle synaptic impairment in the early phase<br>of AD pathology</p>
Repositioning doxycycline for treating synucleinopathies: Evidence from a pre-clinical mouse model
<p>Background and purpose: Parkinson’s disease remains orphan of valuable therapies capable to interfere with the<br>disease pathogenesis despite the large number of symptomatic approaches adopted in clinical practice to manage<br>this disease. Treatments simultaneously affecting α-synuclein (α-syn) oligomerization and neuroinflammation<br>may counteract Parkinson’s disease and related disorders. Recent data demonstrate that Doxycycline, a tetracycline<br>antibiotic, can inhibit α-syn aggregation as well as neuroinflammation. We herein investigate, for the first<br>time, the potential therapeutic properties of Doxy in a human α-syn A53T transgenic Parkinson’s disease mouse<br>model evaluating behavioural, biochemical and histopathological parameters.<br>Experimental approach: Human α-syn A53T transgenic mice were treated with Doxycycline (10 mg/kg daily ip)<br>for 30 days. The effect of treatment on motor, cognitive and daily live activity performances were examined.<br>Neuropathological and neurophysiological parameters were assessed through immunocytochemical, electrophysiological<br>and biochemical analysis of cerebral tissue.<br>Key results: Doxy treatment abolished cognitive and daily life activity deficiencies in A53T mice. The effect on<br>cognitive functions was associated with neuroprotection, inhibition of α-syn oligomerization and gliosis both in<br>the cortex and hippocampus. Doxy treatment restored hippocampal long-term potentiation in association with<br>the inhibition of pro-inflammatory cytokines expression. Moreover, Doxy ameliorated motor impairment and<br>reduced striatal glial activation in A53T mice.<br>Conclusions and implications: Our findings promote Doxy as a valuable multi-target therapeutic approach counteracting<br>both symptoms and neuropathology in the complex scenario of α-synucleinopathies.</p>
Formation and Retrieval of Cell Assemblies in a Biologically Realistic Spiking Neural Network Model of Area CA3 in the Mouse Hippocampus
<p>Dataset accompanying the manuscript "Formation and Retrieval of Cell Assemblies in a Biologically Realistic Spiking Neural Network Model of Area CA3 in the Mouse Hippocampus". This dataset is used to re-create all figure panels with underlying data in the manuscript.</p>
Human-derived fecal microbiota transplantation alleviates mitochondrial dysfunction and social deficits in the BTBR mouse model for autism
<p><span><span>Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition characterized by social communication deficiencies and stereotypic behaviors influenced by hereditary and/or environmental risk factors. There are currently no approved medications for treating the core symptoms of ASD. Human fecal microbiota transplantation (FMT) has emerged as a potential intervention to improve autistic symptoms, but the underlying mechanisms are not fully understood. </span></span><span><span><span><span>In this study, we evaluated the effects of human-derived FMT on behavioral and multi-omics profiles of the BTBR mice, an established model for ASD. FMT effectively alleviated the social deficits in the BTBR mice and normalized their distinct plasma metabolic profile, notably reducing the elevated long-chain acylcarnitines. Integrative analysis linked these phenotypic changes to specific <em>Bacteroides</em> species and vitamin B<sub>6</sub> metabolism. Indeed, vitamin B<sub>6</sub> supplementation improved the social behaviors in BTBR mice. Collectively, these findings shed new light on the interplay between FMT and vitamin B<sub>6</sub> metabolism and revealed a potential mechanism underlying the therapeutic role of FMT in ASD.</span></span></span></span></p>
Fly and mouse tracking models and kinematics related to Anipose toolkit paper
<p>This is a series of datasets related to the Anipose paper. We provide these to allow others to reproduce our tracking results and build upon them.</p> <p>Anipose is an open-source toolkit for robust markerless 3D pose estimation. Anipose is built on the 2D tracking method DeepLabCut, so users can expand their existing experimental setups to obtain accurate 3D tracking. It consists of four components: (1) a 3D calibration module, (2) filters to resolve 2D tracking errors, (3) a triangulation module that integrates temporal and spatial regularization, and (4) a pipeline to structure processing of large numbers of videos.</p> <p>Applying 3D tracking to estimate joint angles of walking <em>Drosophila</em>, we found that flies move their middle legs primarily by rotating their coxa and femur, whereas the front and rear legs are driven primarily by femur-tibia flexion. We then show how Anipose can be used to quantify differences between successful and unsuccessful trajectories in a mouse reaching task.</p> <ul> </ul> <p>We share these fly and mouse datasets and tracking models in this dataset to allow others to reproduce our findings and reuse the training data and models in their research.</p>
Raw western blot from the manuscript "Paradoxical neuronal hyperexcitability in a mouse model of mitochondrial pyruvate import deficiency"
<p>Uncropped western blot associated with the manuscript "Paradoxical neuronal hyperexcitability in a mouse model of mitochondrial pyruvate import deficiency"</p>
Chronic nicotine exposure alters sperm small RNA content in a C57BL/6J mouse model: Implications for epigenetic inheritance
<p>Raw small RNA sequencing data files to accompany manuscript</p>
IMC datasets for HCC mouse models
<p>Raw MCD files associated with published study: Profiling of mouse syngeneic HCC tumor models as a framework to understand anti-PD-1 sensitive tumor microenvironments (<a href="https://doi.org/10.1002/hep.32707">https://doi.org/10.1002/hep.32707</a>)</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.