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opencc-by-4.0Oct 2024View details →

High-throughput behavioural phenotyping of 25 C. elegans disease models including patient-specific mutations

This repository contains: all code, phenomic data, extracted features, calculated stats, normalised z-scores and timerseries data for all of the disease mutant phenologs and data in our paper: High-throughput behavioural phenotyping of 25 C. elegans disease models including patient-specific mutations.

opencc-by-4.0Oct 2024View details →

Systemic inflammation accelerates neurodegeneration in a rat model of Parkinson's disease overexpressing human alpha synuclein

Parkinson’s disease (PD) involves genetic and environmental risk factors. Increasing research efforts have been made to understand how they interact to impair homeostasis and elevate risk. Inflammation could be one unifying factor. In this study, wild-type (WT) and overexpressing human α-synuclein (Snca+/+) rats were intraperitoneally injected with a single dose of lipopolysaccharide (LPS) or with saline (SAL). In these animals we assessed the development of PD-like symptoms by immunohistology, high-dimensional flow cytometry, electrophysiology, and behavioral analyses. A single injection of LPS to both WT and Snca+/+ rats triggered long-lasting increased activation of pro-inflammatory microglial markers, infiltrating monocytes and T-lymphocytes. However, only LPS Snca+/+ rats displayed dopaminergic neuronal loss in the substantia nigra pars compacta (SNpc), associated with a reduction of evoked dopamine release in the striatum. No significant changes were observed in the behavioral domain.

opencc-by-4.0Nov 2024View details →

Replication files for: Integrative modeling of the spread of serious infectious diseases and corresponding wastewater dynamics

This repository contains the inputs used and outputs produced by the urban water management modelling software ++SYSTEMS for the paper Integrative Modeling of the Spread of Serious Infectious Diseases and Corresponding Wastewater Dynamics. It includes the following files: <ol> <li>simulation_output.zip:</li> <ol> <li>In the subfolder infection_model, .csv and .txt files containing the agent-based model outputs for 250 simulations with homogeneous infection initialisation (2024_09_17) or localised infection initialisation (2024_10_15). These files were used as inputs for ++SYSTEMS.</li> <li>In the subfolder wastewater_model, .txt files containing the flow rates by pipe and the viral concentrations by sampling location for each combination of ABM simulation and rain/decay scenario. These files were the outputs of ++SYSTEMS.</li> </ol> <li>S1_INSIDe_Demonstrator_AreaList.txt: .txt file defining the area types and number of inhabitants for each surface area within the synthetic neighbourhood used in the paper. This file was also used as an input for ++SYSTEMS. </li> <li>S2_systems_model_files.zip: .csv files defining the characteristics of the sewage system for the synthetic neighbourhood as well as the rain scenarios used in the paper. These file were also used as inputs for ++SYSTEMS. </li> </ol>

opencc-zeroAug 2021View details →

STonKGs Disease Model

The fine-tuned model trained on disease annotations.

opencc-by-4.0Sep 2021View details →

Metabolic Derangement in Polycystic Kidney Disease Mouse Models Is Ameliorated by Mitochondrial-Targeted Antioxidants

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressively enlarging cysts. Here we elucidate the interplay between oxidative stress, mitochondrial dysfunction, and metabolic derangement using two mouse models of PKD1 mutation, PKD1RC/null and PKD1RC/RC. Mouse kidneys with PKD1 mutation have decreased mitochondrial complexes activity. Targeted proteomics analysis shows a significant decrease in proteins involved in the TCA cycle, fatty acid oxidation (FAO), respiratory complexes, and endogenous antioxidants. Overexpressing mitochondrial-targeted catalase (mCAT) using adeno-associated virus reduces mitochondrial ROS, oxidative damage, ameliorates the progression of PKD and partially restores expression of proteins involved in FAO and the TCA cycle. In human ADPKD cells, inducing mitochondrial ROS increased ERK1/2 phosphorylation and decreased AMPK phosphorylation, whereas the converse was observed with increased scavenging of ROS in the mitochondria. Treatment with the mitochondrial protective peptide, SS31, recapitulates the beneficial effects of mCAT, supporting its potential application as a novel therapeutic for ADPKD.

opencc-by-4.0Jan 2023View details →

KidDO project update - quantitative proteomic and metabolomic analysis of five mouse models with chronic kidney disease

Chronic kidney disease (CKD) is one of the most deadly diseases faced by patients and is a major global health and socioeconomic burden.CKD increases cardiovascular morbidity and premature mortality and decreases quality of life. Hypertension (HTN) and type 2 diabetes mellitus (T2DM), which are reaching epidemic levels, are major risk factors for CKD. CKD diagnosis and progression is based on estimated GFR (eGFR) and urinary albumin excretion. However, eGFR only has a predictive value in advanced disease and there is risk of progressive CKD in non-albuminuric individuals. Thus, there is an urgent need for new approaches for early detection of the most “at risk” individuals and identification of CKD signatures to aid in designing novel drugs and preventive measures that could ameliorate progression of CKD. Our overarching goal is to identify metabolites that predict kidney cell phenotypes during CKD and how crosstalk of these metabolites with the proteome drive CKD progression. We will integrate metabolomics and proteomic information from animal models of CKD with human CKD patient biopsies to identify common signatures in the tubulointerstitium that correlate with human pathophysiology. Here we provide quantitative proteomic and metabolomic datasets, as well as plasma and urine electrolyte measurements on five CKD mouse models.

opencc-by-4.0Nov 2022View details →

Modeling the Sequence Dependence of Differential Antibody Binding in the Immune Response to Infectious Disease

Raw peptide microarray data of fluorescence intensities representing relative binding of antibodies in sera samples collected from different cohorts of patients diagnosed with a number of viral infections. Healthy controls are also included. Columns: Sequence - peptide sequence HCV - Hepatitis Virus C Dengue - Dengue virus WNV - West Nile Virus HBV - Hepatitis Virus B Chagas - Chagas disease ND - negative/healthy donor LowCV - low coefficient of variation HighCV - high coefficient of variation

opencc-zeroMar 2023View details →

Ex vivo 100 μm isotropic diffusion MRI‐based tractography of connectivity changes in the end‐stage R6/2 mouse model of Huntington's disease

<div> <div> <div> <div> Background: Huntington's disease is a progressive neurodegenerative disorder. Brain atrophy, as measured by volumetric magnetic resonance imaging (MRI), is a downstream consequence of neurodegeneration, but microstructural changes within brain tissue are expected to precede this volumetric decline. The tissue microstructure can be assayed non-invasively using diffusion MRI, which also allows a tractographic analysis of brain connectivity. Methods: We here used ex vivo diffusion MRI (11.7T) to measure microstructural changes in different brain regions of end‐stage (14 weeks of age) wild type and R6/2 mice (male and female) modeling Huntington's disease. To probe the microstructure of different brain regions, reduce partial volume effects and measure connectivity between different regions, a 100 μm isotropic voxel resolution was acquired. Results: Although fractional anisotropy did not reveal any difference between wild‐type controls and R6/2 mice, mean, axial, and radial diffusivity were increased in female R6/2 mice and decreased in male R6/2 mice. Whole brain streamlines were only reduced in male R6/2 mice, but streamline density was increased. Region‐to‐region tractography indicated reductions in connectivity between the cortex, hippocampus, and thalamus with the striatum, as well as within the basal ganglia (striatum—globus pallidus—subthalamic nucleus—substantia nigra—thalamus). Conclusions: Biological sex and left/right hemisphere affected tractographic results, potentially reflecting different stages of disease progression. This proof‐of‐principle study indicates that diffusion MRI and tractography potentially provide novel biomarkers that connect volumetric changes across different brain regions. In a translation setting, these measurements constitute a novel tool to assess the therapeutic impact of interventions such as neuroprotective agents in transgenic models, as well as patients with Huntington's disease. </div> </div> </div> </div>

opencc-by-4.0Jun 2023View details →

Monitoring of postpartum body condition at the cow and herd levels: assessing explanatory and predictive power of disease risk models

Objectives 1- To define the herd threshold for cows with poor body condition based on its predictive capacity for disease risk at the herd level, and 2- to estimate the impact measures on disease rates due to body condition indicators in transition period. Two commercial grazing dairy herds (Herd A=5.034 and herd B=7.965 lactations) from Argentinean Pampa region were used to perform a longitudinal retrospective study during a 4-year period (2014 –2017).Health, reproductive and body condition score (BCS) records were gathered. The BCS (5-point scale) was performed at calving and at the time of reproductive release. The difference between both measures of BCS was used to assess the body condition loss (∆BCS). All the cows not bred by 70 DIM were checked for anestrus.Calving cohorts of 21-day were defined at each herd and parity group through the entire study period. The frequency of cows with BCS<3 or ∆BC>-0.5 at each cohort were calculated and used to define quartiles through whole study period. Quartiles were used, one at a time, as threshold to dichotomize the cohorts to predict the risk that a cohort has a frequency of anestrus over the median.The higher AUC was used as selection criterium to determine the herd level threshold at each HERD and PARITY level. The population attributable fraction (AFP) of anestrus rate to body condition indicators at each cohort was calculated, for every HERD and PARITY level.

opencc-zeroSep 2023View details →

Dataset: Disease-associated KCNMA1 variants decrease circadian clock robustness in channelopathy mouse models

KCNMA1 encodes the voltage- and calcium-activated K+ (BK) channel, which regulates suprachiasmatic nucleus (SCN) neuronal firing and circadian behavioral rhythms. Gain-of-function (GOF) and loss-of-function (LOF) alterations in BK channel activity disrupt circadian behavior, but the effect of human disease-associated KCNMA1 channelopathy variants has not been studied on clock function. Here, we assess circadian behavior in two GOF and one LOF mouse lines. Heterozygous Kcnma1N999S/WT and homozygous Kcnma1D434G/D434G mice are validated as GOF models of paroxysmal dyskinesia (PNKD3), but whether circadian rhythm is affected in this hypokinetic locomotor disorder is unknown. Conversely, homozygous LOF Kcnma1H444Q/H444Q mice do not demonstrate PNKD3. We assessed circadian behavior by locomotor wheel running activity. All three mouse models were rhythmic, but Kcnma1N999S/WT and Kcnma1D434G/D434G showed reduced circadian amplitude and decreased wheel activity, corroborating prior studies focused on acute motor coordination. In addition, Kcnma1D434G/D434G mice had a small decrease in period. However, the phase-shifting sensitivity for both GOF mouse lines was abnormal. Both Kcnma1N999S/WT and Kcnma1D434G/D434G mice displayed increased responses to light pulses and took fewer days to re-entrain to a new light:dark cycle. In contrast, the LOF Kcnma1H444Q/H444Q mice showed no difference in any of the circadian parameters tested. The enhanced sensitivity to phase-shifting stimuli in Kcnma1N999S/WT and Kcnma1D434G/D434G mice was similar to other Kcnma1 GOF mice. Together with previous studies, these results suggest that increasing BK channel activity decreases circadian clock robustness, without rhythm ablation.

restrictedIPD-UNDECIDEDFeb 2026View details →

Real-PD Trial: Development of Clinical Prognostic Models for Parkinson's Disease

ClinicalTrials.gov study NCT02474329. IPD Sharing: Not stated. Countries: 1. Publications: 9.

controlledIPD-YESFeb 2026View details →

Using Clinical Prediction Models to Improve Treatment for Patients With Chronic Obstructive Pulmonary Disease (COPD)

ClinicalTrials.gov study NCT05309356. IPD Sharing: YES. Countries: 1. Publications: 1.

closedIPD-NOFeb 2026View details →

Coronary Imaging and Metabolic Indicators-Based Risk Prediction Model for Coronary Artery Disease(CMI-RiskCAD)

ClinicalTrials.gov study NCT07353762. IPD Sharing: NO. Countries: 1. Publications: 1.

closedIPD-NOFeb 2026View details →

Volatilome and Single-Lead Electrocardiogram Optimize Ischemic Heart Disease Diagnosis Using Machine Learning Models

ClinicalTrials.gov study NCT06181799. IPD Sharing: NO. Countries: 1. Publications: 8.

restrictedIPD-UNDECIDEDFeb 2026View details →

A Study to Evaluate BMS-986141 Added on to Aspirin or Ticagrelor or the Combination, on Thrombus Formation in a Thrombosis Chamber Model in Participants With Stable Coronary Artery Disease and Healthy

ClinicalTrials.gov study NCT05093790. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →

A Chronic Care Model Based Quality Improvement (QI) Program to Improve the Care of Patients With Chronic Kidney Disease (CKD)

ClinicalTrials.gov study NCT01290614. IPD Sharing: Not stated. Countries: 1. Publications: 2.

publicSep 2023View details →

Dataset: Disease-associated KCNMA1 variants decrease circadian clock robustness in channelopathy mouse models

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publicAug 2025View details →

Microglial replacement in a Sandhoff disease mouse model reveals myeloid-derived β- hexosaminidase is necessary for neuronal health

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publicAug 2024View details →

A therapeutic small molecule enhances γ-oscillations and improves cognition/memory in Alzheimer’s disease model mice

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