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1,274 results for “disease models”
Statistical analysis code for output from a model used to simulate foot-and-mouth disease dynamics in the United Kingdom
<p>Epidemics can sometimes be managed through reductions of host density, such as social distancing for human diseases, reducing plant density through cultural and genetic means, and host culling for epizootics. These approaches allow for a certain density of hosts to remain within a targeted area. By contrast, total ring depopulation is often used as a management strategy for emerging infectious diseases in livestock. In this study, we explore the trade-offs of a density-based culling strategy to determine if fewer livestock farms can be culled within rings while maintaining a decrease in disease transmission. To do so, we evaluated a farm-density-based ring culling strategy to control foot-and-mouth disease (FMD) in the United Kingdom. This strategy may allow for some farms within rings around infected premises (IPs) to escape depopulation, with the aim to prevent over-culling during outbreaks. Using a spatially-explicit, stochastic, state-transition simulation algorithm originally developed by Keeling et al. 2001 to model FMD spread in the United Kingdom, we simulated this reduced-farm-density, or "target density" strategy. We modeled FMD disease spread in four counties in the UK (Aberdeenshire, Cumbria, Devon, and North Yorkshire) that have different farm demographies. We ran 740,000 simulations in a full-factorial analysis of epidemic impact measurements (i.e. culled animals, culled farms, epidemic length) and cull strategy parameters (i.e. target farm density, daily farm cull capacity, cull radius). We found that all of the cull strategy parameters were drivers of epidemic impact. We found that outbreaks in Cumbria had higher epidemic impacts and were more likely to take off compared with other counties with more outbreaks being likely to take off in Cumbria. Most importantly, in all counties, our proposed target density strategy was more effective at combatting FMD compared with traditional 'total ring depopulation' when considering average culled animals and culled farms. The differences in epidemic impact between the counties are likely driven by farm demography, especially differences in cattle and farm density. This target density strategy can be applied to many different systems, including other livestock and agricultural systems, to reduce host density as opposed to over-culling hosts.</p>
Dihydrosphingolipids are associated with steatosis and increased fibrosis damage in human and animal models of non-alcoholic fatty liver disease
<p>Data sets used for the article entitled: "Accumulation of dihydrosphingolipids and neutral lipids is related to steatosis and fibrosis damage in human and animal models of non-alcoholic fatty liver disease"</p> <p>- Patient data: DATA Patients JLR.xlsx</p> <p>- Mouse data: DATA Mice.xlsx</p>
Celluloepidemiology: a novel paradigm for quantifying infectious disease dynamics through T-cell modelling on a population level
<p>T-cell receptor sequencing (TCR-seq) was performed on enriched CD8+ T-cells. TCR clonotype annotation was performed using MiXCR v.3.0.13 with the default input parameters.</p> <p>Full origin and method description available in:<br>Celluloepidemiology: a novel paradigm for quantifying infectious disease dynamics through T-cell modelling on a population level</p>
Improving distribution models of sparsely-documented disease vectors by incorporating information on related species via joint modeling
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Impact of infectious diseases on wild bovidae populations in Thailand: Insights from population modelling and disease dynamics
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Know what you don't know: Embracing state uncertainty in disease-structured multistate models
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Statistical analysis code for output from a model used to simulate foot-and-mouth disease dynamics in the United Kingdom
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Novel disease state model finds most juvenile green turtles develop and recover from fibropapillomatosis
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Data from: Longitudinal three-photon imaging for tracking amyloid plaques and vascular degeneration in a mouse model of Alzheimer’s disease
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Longitudinal analysis of the microbiome and metabolome in the 5xfAD mouse model of Alzheimer's disease
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Raw data to "Blunting neuroinflammation with resolvin D1 prevents early pathology in a rat model of Parkinson's disease"
<p>Background: In vivo treatment of animals with anti-inflammatory and pro-resolving mediators (SPMs) could be counteracted by their limited in vivo bioavailability due to their unstable nature as lipids that can undergo oxidation or enzymatic degradation.</p> <p>Results: Thus, we performed a time course of RvD1 plasma levels over 36 hours after an initial intraperitonael injection of this lipid mediator at a concentration of 200 ng/animal. After a single injection the plasma concentration of RvD1 peaked at 1h (~360 pg/ml), stayed almost constant at 3h(~360 pg/ml), halved its levels after 6h (~180 pg/ml) and slowly returned close to the baseline after 36h (~30 pg/ml). These results indicate that RvD1 is rapidly distributed into the bloodstream and eliminated from the vascular compartment due to metabolism and/or diffusion into the blood–brain barrier.</p> <p>Conclusions: These findings are important to define route and timing of in vivo administration of SPMs in order to maintain sufficient levels to sustain biological activities both in the periphery and within the central nervous system.</p>
Data from: Sleep, inflammation, and cognitive behavior of aged wild-type mice subjected to diffuse brain injury and aged 3xTg-AD mice as a model of Alzheimer's disease
<p>Identifying differential responses between sexes following traumatic brain injury (TBI) can elucidate the mechanisms behind disease pathology. Peripheral and central inflammation in the pathophysiology of TBI can increase sleep in male rodents, but this remains untested in females. We hypothesized that diffuse TBI would increase inflammation and sleep in males more so than in females. Diffuse TBI was induced in C57BL/6J mice and serial blood samples were collected (baseline, 1, 5, 7 days post‐injury [DPI]) to quantify peripheral immune cell populations and sleep regulatory cytokines. Brains and spleens were harvested at 7DPI to quantify central and peripheral immune cells, respectively. Mixed‐effects regression models were used for data analysis. Female TBI mice had 77%–124% higher IL‐6 levels than male TBI mice at 1 and 5DPI, whereas IL‐1β and TNF‐α levels were similar between sexes at all timepoints. Despite baseline sex differences in blood‐measured Ly6Chigh monocytes (females had 40% more than males), TBI reduced monocytes by 67% in TBI mice at 1DPI. Male TBI mice had 31%–33% more blood‐measured and 31% more spleen‐measured Ly6G+ neutrophils than female TBI mice at 1 and 5DPI, and 7DPI, respectively. Compared with sham, TBI increased sleep in both sexes during the first light and dark cycles. Male TBI mice slept 11%–17% more than female TBI mice, depending on the cycle. Thus, sex and TBI interactions may alter the peripheral inflammation profile and sleep patterns, which might explain discrepancies in disease progression based on sex.</p>
Mechanical stimulation prevents impairment of axon growth and overcompensates microtubules destabilization in cellular models of Alzheimer's disease related Tau pathology
<p>Data and metadata associated to a publication 10.3389/fmed.2025.1519628</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>
Cross-disease integration of single-cell RNA sequencing data from lung myeloid cells reveals TAM signature in in vitro model
<p>Single cells from a 3D human cell-based model comprising tumor cell line-derived spheroids, cancer-associated fibroblasts and primary monocytes were dissociated and analyzed using scRNAseq. 4 monocyte donors were used in the 3D model, and 3 monocyte donors were used for 2D differentiation of macrophages.</p>
IMBALANCED MACHINE LEARNING CLASSIFICATION MODELS FOR REMOVAL BIOSIMILAR DRUGS AND INCREASED ACTIVITY IN PATIENTS WITH RHEUMATIC DISEASES
<p>Objective: Predict long-term disease worsening and the removal of biosimilar medication in patients with rheumatic diseases.</p><p>Methodology: Observational, retrospective, and descriptive study. Review of a database of patients with immune-mediated inflammatory rheumatic diseases. Disease worsening and removing biosimilars are imbalanced variables, that require using imbalanced machine learning models selected based on their superior f1-scores and great accuracy. Previously, we selected the most important variables using mutual information tests.</p><p>Results: The best imbalanced machine learning models to predict disease worsening and the removal of the biosimilar obtained f1-scores of 0.52 and 0.63, respectively. Both models are decision trees. In the first one, two important factors are switching of biosimilar and age, and in the second, the relevant variables are optimization and the value of the initial CRP. </p><p>Conclusions: Biosimilar drugs do not always work well for rheumatic diseases. We obtained two imbalanced machine learning models to detect those cases, where the drug should be removed or where the activity of the disease increases from low to high. Our decision trees use variables, such as age or switching, not considered in previous studies.</p>
Enhanced mTORC1 signaling and protein synthesis in pathologic alpha-synuclein cellular and animal models of Parkinson's disease
<p>Pathologic alpha-synuclein plays an important role in the pathogenesis of alpha-synucleinopathies such as Parkinson's disease (PD). Disruption of proteostasis is thought to be central to pathologic alpha-synuclein (alpha-syn) toxicity; however, the molecular mechanism of this deregulation is poorly understood. Here we report that pathologic alpha-syn activates the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) leading to enhanced mRNA translation via binding tuberous sclerosis protein (TSC) 2 and destabilizing the TSC1-TSC2 complex. Genetic and pharmacologic inhibition of mTOR and protein synthesis rescue the dopamine neuron loss, behavioral deficits, and aberrant biochemical signaling in the alpha-syn preformed fibril (PFF) and Drosophila alpha-syn transgenic models of pathologic alpha-syn induced degeneration. Our findings establish a potential molecular mechanism by which pathologic alpha-syn activates mTORC1 leading to enhanced protein synthesis and concomitant neurodegeneration in PD.</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>
Modelling data for: Short-course combination treatment for experimental chronic Chagas disease
<p><span>Chagas disease, caused by the protozoan parasite <em>Trypanosoma</em> <em>cruzi</em>, affects millions of people in the Americas and across the world leading to considerable morbidity and mortality. Current treatment options, benznidazole (BNZ) and nifurtimox, offer limited efficacy and often lead to adverse side effects due to long treatment durations. Better treatment options are therefore urgently required. Here we describe a pyrrolopyrimidine series, identified through phenotypic screening, that offers a clear opportunity to improve on current treatments. In vitro cell-based washout assays demonstrate that compounds in the series are incapable of killing all parasites, however, combining these pyrrolopyrimidines with a sub-efficacious dose of BNZ can clear all parasites in vitro after five days. Importantly, these findings were replicated in a clinically predictive<em> in vivo</em> model of chronic Chagas disease, where five days of treatment with the combination was sufficient to prevent parasite relapse. Comprehensive mechanism of action studies, supported by ligand-structure modelling, show that compounds from this pyrrolopyrimidine series inhibit the Q</span><sub><span>i</span></sub><span> active site of <em>T. cruzi</em> cytochrome <em>b</em>, part of the cytochrome <em>bc1</em> complex of the electron transport chain. Knowledge of the molecular target enabled a cascade of assays to be assembled to evaluate selectivity over the human cytochrome <em>b</em> homologue. As a result, a highly selective and efficacious lead compound was identified. The combination of our lead compound with BNZ rapidly clears<em> T. cruzi</em> parasites, both <em>in vitro</em> and <em>in vivo</em>, and shows great potential to overcome key issues associated with currently available treatments. </span></p>
Model of a diseased eye
A list describing the various pathologies. This eye could be a model of allergic conjunctivitis. From the collection of the museum library at the UCL institute of ophthalmology. Source: Objaverse 1.0 / Sketchfab
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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.