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34,778 results for “diseases”
Occupational Lyme Disease: A Systematic Review and Meta-Analysis
<p>Data used in meta-analysis</p>
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>
A Diagnostic Classifier for Gene Expression-Based Identification of Early Lyme Disease
<p>This data repository contains the source code and pertinent training and test data sets used in the manuscript, <em>A Diagnostic Classifier for Gene Expression-Based Identification of Early Lyme Disease</em>. </p>
Immune disease risk variants regulate gene expression dynamics during CD4+ T cell activation
<p>During activation, T cells undergo extensive changes in gene expression which shape the properties of cells to exert their effector function. Therefore, understanding the genetic regulation of gene expression during T cell activation provides essential insights into how genetic variants influence the response to infections and immune diseases. We generated a single-cell map of expression quantitative trait loci (eQTL) across a T cell activation time-course. We profiled 655,349 CD4+ naive and memory T cells, capturing transcriptional states of unstimulated cells and three time points of cell activation in 119 healthy individuals. We identified 38 cell clusters, including stable clusters such as central and effector memory T cells and transient clusters that were only present at individual time points of activation, such as interferon-responding cells. We mapped eQTLs using a T cell activation trajectory and identified 6,407 eQTL genes, of which a third (2,265 genes) were dynamically regulated during T cell activation. We integrated this information with GWAS variants for immune-mediated diseases and observed 127 colocalizations, with significant enrichment in dynamic eQTLs. Immune disease loci colocalized with genes that are involved in the regulation of T cell activation, and genes with similar functions tended to be perturbed in the same direction by disease risk alleles. Our results emphasize the importance of mapping context-specific gene expression regulation, provide insights into the mechanisms of genetic susceptibility of immune diseases, and help prioritize new therapeutic targets.</p> <p>This dataset comprises of summary stats for eQTLs identified in the study (parquet files) and the ones which passed significance threshold (tensor_out.tar.gz archive). Files are described by cell subset (CD4 Naive, CD 4 Memory, TEMRA, TCM, etc.), time since activation (16h, 4h, 5days) as described in the publication (preprint https://doi.org/10.1101/2021.12.06.470953)</p>
The indirect impact of COVID-19 on major clinical outcomes of people with Parkinson's disease or atypical parkinsonism: a cohort study. Raw data
<p>Raw dataset of the study "The indirect impact of COVID-19 epidemic on major clinical outcomes of people with Parkinson’s disease (PD) or atypical parkinsonism: a cohort study"</p>
Data from: Cascading effects of a disease outbreak in a remote protected area
<p>Disease outbreaks induced by humans increasingly threaten wildlife communities worldwide. Like predators, pathogens can be key top-down forces in ecosystems, initiating trophic cascades that may alter food webs. An outbreak of mange in a remote Andean protected area caused a dramatic population decline in a mammalian herbivore (the vicuña), creating conditions to test the cascading effects of disease on the ecological community. By comparing a suite of ecological measurements to pre-disease baseline records, we demonstrate that mange restructured tightly-linked trophic interactions previously driven by a mammalian predator (the puma). Following the mange outbreak, scavenger (Andean condor) occurrence in the ecosystem declined sharply and plant biomass and cover increased dramatically in predation refuges where herbivory was historically concentrated. The evidence shows that a disease-induced trophic cascade, mediated by vicuña density, could supplant the predator-induced trophic cascade, mediated by vicuña behavior, thereby transforming the Andean ecosystem. </p>
Meta-analysis defines predominant shared microbial responses in various diseases and a specific inflammatory bowel disease signal
<p>Datasets and analysis notebooks for recreating the analysis described in the paper.</p> <p>biom tables of the original datasets used in the meta-analysis are not included due to privacy issues. Instead, we include the biom table containing the NRMD for each study/ASV</p> <p>Updated data and notebooks can also be found at the github page: </p> <p><a href="https://github.com/amnona/paper-metaanalysis">https://github.com/amnona/paper-metaanalysis</a></p> <p>NOTE: files here are provided in a per-directory .zip file in order to preserve internal directory structure.</p> <p> </p>
Processed FDG-PET data from: A computational model of neurodegeneration in Alzheimer's disease
<p>Disruption of mental functions in Alzheimer's disease (AD) and related disorders is accompanied by selective degeneration of brain regions. These regions comprise large-scale ensembles of cells organized into systems for mental functioning, however the relationship between clinical symptoms of dementia, patterns of neurodegeneration, and functional systems is not clear. We developed a model of the association between dementia symptoms and degenerative brain anatomy using F18-fluorodeoxyglucose (FDG) PET and dimensionality reduction techniques patients with AD. This data and code package contains preprocessed FDG-PET images from 423 subjects across the Alzheimer's disease spectrum and the MATLAB code to produce eigenbrains from this data.</p>
Data from: Comparing the efficacy of control strategies for infectious disease outbreaks using field and simulation studies
<p>Diseases characterized by long distance inoculum dispersal (LDD) are among the fastest spreading epidemics in both natural and managed landscapes. Management of such epidemics is extremely challenging because of asymptomatic infection extending at large spatial scales and frequent escape from the newly established disease sources. We compared the efficacy of area- and timing-based disease management strategies in artificially initiated field epidemics of wheat stripe rust and complemented with simulations from an updated version of the spatially explicit model EPIMUL, using model parameters relevant to field epidemics. The model was further used to expand the number of epidemic mitigations beyond that feasible to incorporate in the field. The field experiment was conducted for two years in two locations having different climatic conditions. Culling and protection treatments were applied at different times after epidemic initiation and to different spatial extents surrounding the outbreaks. In each experiment, treatments were replicated four times in plots 33.5 m long and 1.52 m wide with a 0.76 x 0.76 m inoculated focus centered within each plot. Disease gradients were assessed along the center lines of the plots at 1.52 m intervals both upwind and downwind from the focus. Both field and simulation results indicated that control measures applied over the entire population were highly effective in suppressing the epidemics by more than 99% but may not always be logistically and economically feasible at large spatial scales. Comparison between the variable sized treatment areas and application timings suggested that implementing contiguous premises (CP) cull at 1 day after first sporulation in the outbreak focus reduced rust by 52 and 60% in Corvallis and Madras, respectively. However, altering the cull size did not significantly affect the disease epidemic development, which suggested that early timing had a greater influence in suppressing the epidemics than did increased area of application. However, sufficiently large, treated areas may compensate for a delay in application timing to some extent. Results from these replicated treatments may help to devise appropriate management strategies for other LDD pathogens. </p>
Genetic modifiers of Huntington's disease differentially influence motor and cognitive domains
<p class="MsoNormal"><span>Genome-wide association studies (GWAS) of Huntington's disease (HD) have identified six DNA maintenance gene loci (among others) as modifiers and implicated a two step-mechanism of pathogenesis: somatic instability of the causative HTT CAG repeat with subsequent triggering of neuronal damage. The largest studies have been limited to HD individuals with a rater-estimated age at motor onset. To capitalize on the wealth of phenotypic data in several large HD natural history studies, we have performed algorithmic prediction using common motor and cognitive measures to predict age at other disease landmarks as additional phenotypes for GWAS. Combined with imputation using the Trans-Omics for Precision Medicine reference panel, predictions using integrated measures provided objective landmark phenotypes with greater power to detect most modifier loci. Importantly, substantial differences in the relative modifier signal across loci, highlighted by comparing common modifiers at MSH3 and FAN1, revealed that individual modifier effects can act preferentially in the motor or cognitive domains. Individual components of the DNA maintenance modifier mechanisms may therefore act differentially on the neuronal circuits underlying the corresponding clinical measures. In addition, we identified new modifier effects at the PMS1 and PMS2 loci and implicated a potential new locus on chromosome 7. These findings indicate that broadened discovery and characterization of HD genetic modifiers based on additional quantitative or qualitative phenotypes offers not only the promise of in-human validated therapeutic targets, but also a route to dissecting the mechanisms and cell types involved in both the somatic instability and toxicity components of HD pathogenesis.</span></p>
Raw data for "Effect of MRgFUS treatment on cortical activity in Parkinson's disease: a fNIRS study"
<p>In this paper, a new combined approach, based on Magnetic Resonance-guided Focused Ultrasound Surgery (MRgFUS) technique and functional Near Infrared Spectroscopy (fNIRS), was applied for treatment and monitoring of patients affected by bilateral Parkinson’s disease (PD). On one side, MRgFUS enables non-invasive thalamotomy by combining FUS for tissue ablation and MR for targeting and monitoring. On the other side, fNIRS allows to monitor, non-invasively and without strict motion restriction even in a daily life environment, cortical neural activity related dynamics of both oxygenated and deoxygenated haemoglobin (HbO and HbR, respectively). In particular, the changes of cortical activation pattern in PD patients, with respect to age matched healthy control subjects, were analysed, while performing left and right hand finger tapping (LFT and RFT, respectively), before MRgFUS treatment, and at two different time intervals after the treatment. By comparison with the pre-treatment session, significant activations were predominantly observed one week after the treatment, with patterns recalling those of control group, and partially lost one month later, likely because of the neurodegenerative nature of PD. In addition, activations were more marked for LFT task, being the treatment performed on the right hemisphere. These results appear promising in view of the application of fNIRS for neurorehabilitation, especially in those clinical settings where traditional neuroimaging techniques cannot be applied.</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>
Factors associated with coronary heart disease in COPD patients and controls
<p><strong><span>Background</span></strong></p> <p><span>COPD and coronary heart disease (CHD) frequently co-occur, yet which COPD phenotypes are most prone to CHD is poorly understood. </span><span>The aim of this study was to see whether COPD patients did have a true higher risk for CHD than subjects without COPD, and to examine a range of potential factors associated with CHD in COPD patients and controls</span></p> <p><strong><span>Methods</span></strong></p> <p><span>347 COPD patients and 428 non-COPD controls, were invited for coronary computed tomography angiography (CCTA) and pulmonary CT. Arterial blood gas, bioelectrical impedance and lung function was measured, and a detailed medical history taken. The CCTA was evaluated for significant coronary stenosis and calcium score (CaSc), and emphysema defined as >10% of total area <-950 Hounsfield units. </span></p> <p><strong><span>Results</span></strong></p> <p><span>12.6% of the COPD patients and 5.7% of the controls had coronary stenosis (p<0.01), whereas 55.9% of the COPD patients had a CaSc>100 compared to 31.6% of the controls (p<0.01). In a multivariable model adjusting for sex, age, body composition, pack-years, CRP, cholesterol/blood pressure lowering medication use and diabetes mellitus, the OR (95% CI) for having significant stenosis was 1.80 (0.86-3.78) in COPD patients compared with controls. In a similar model, the OR (95% CI) for having CaSc>100 was 1.68 (1.12-2.53) in COPD patients compared with controls. Examining the risk of significant stenosis and CaSc>100 among COPD patients, no variable was associated with significant stenosis, whereas male sex [OR 2.85 (1.56-5.21)], age [OR 3.74 (2.42-5.77)], statin use [OR 2.23 (1.23-4.50)] were associated with CaSc>100, after adjusting for body composition, pack-years, C-reactive protein, use of angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), diabetes, emphysema score, GOLD category, exacerbation frequency, eosinophilia, and hypoxemia.</span></p> <p><strong><span>Conclusion</span></strong></p> <p><span>COPD patients were more likely to have CHD, but neither emphysema score, lung function, exacerbation frequency, nor hypoxemia predicted presence of either coronary stenosis or CaSc>100. </span></p>
Synthesis of batrachochytrium dendrobatidis infection in South America: amphibian species under risk and areas to focus research and disease mitigation
<p>Amphibian chytridiomycosis, caused by Batrachochytrium dendrobatidis (Bd), has been recognized as the infectious disease causing the most catastrophic loss of biodiversity known to science, with South America being the most impacted region. We tested whether Bd prevalence is distributed among host taxonomy, ecoregion, conservation status and habitat preference in South America. Here we provide a synthesis on the extent of Bd infection across South America based on 21,648 molecular diagnostic assays, roles of certain species in the epidemiology of Bd and explore its association with the reported amphibian catastrophic declines in the region. We show that Bd is widespread, with a continental prevalence of 23.2%. Its occurrence in the region shows a phylogenetic signal and the probability of infection is determined by ecoregion, preferred habitat, and extinction risk hosts' traits. The taxa exhibiting highest Bd occurrence, were mostly aquatic amphibians, including Ranidae, Telmatobiidae, Hylodidae, Calyptocephalellidae and Pipidae. Surprisingly, families exhibiting unusually low Bd prevalence included species in which lethal chytridiomycosis and population declines have been described (genus Atelopus, Rhinoderma and Eleutherodactylus). Higher than expected prevalence of Bd occurred mainly in amphibians living associated with mountain environments in the Andes and Atlantic forests, reflecting highly favourable Bd habitats in these areas. Invasive amphibian species (e.g. Lithobates catesbeianus and Xenopus laevis) exhibited high Bd prevalence, as thus we suggest using these as sentinels to understand their potential role as reservoirs, vectors or spreaders of Bd that can be subjected to management. Our results guide on the prioritization of conservation actions to prevent further biodiversity loss due to chytridiomycosis in the world's most amphibian diverse region.</p>
Hormone receptors AR, ER, PR and growth factor receptor Her-2 expression in oral squamous cell carcinoma: Correlation with overall survival, disease-free survival and 10-year survival in a high-risk population
<p>Oral squamous cell carcinoma (OSCC) comprises most of head and neck neoplasms and is one of the highest-ranking and lethal cancers in Pakistan due to prevailing mouth habits. Growth and hormonal receptors act as prognostic markers and targets for therapy in some cancers, but their application in OSCC is largely unexplored. This study aimed to evaluate the expression of growth and hormonal receptors in OSCC patients and correlate it with 10-year, overall and disease-free survival. To achieve this objective, immunohistochemistry for Her-2, AR, ER and PR was performed on 100 formalin-fixed paraffin-embedded primary OSCC specimens. Receptor expression was correlated with mouth habits and clinicopathological features and patient survival was analyzed using Kaplan-Meier method and Cox regression univariate analysis. We observed that in 100 patients, there were 57 males and 43 females. Immunopositive Her-2 expression was observed in 21% of patients, AR in 13%, ER in 3% and 0% for PR. Patients with betel quid/areca nut mouth habits had significantly absent Her-2 expression (P=0.035). Also, Her-2 negative patients were also negative for AR expression (P=0.002). Her-2 positive patients had poor 10-year survival (P=0.041). A trend of low survival and high recurrence rate was observed in AR positive patients, but this was not significant (P=0.072). No statistically relevant correlations were seen in the case of ER and PR. In conclusion, Her-2 may be a valuable marker for predicting long-term prognosis of OSCC patients.</p>
Complex feline disease mapping using a dense genotyping array
<p>The current feline genotyping array of 63k single nucleotide polymorphisms has proven its utility within breeds, and its use has led to the identification of variants associated with Mendelian traits in purebred cats. However, compared to single gene disorders, association studies of complex diseases, especially with the inclusion of random bred cats with relatively low linkage disequilibrium, require a denser genotyping array and an increased sample size to provide statistically significant associations. Here, we undertook a multi-breed study of 1,122 cats, most of which were admitted and phenotyped for nine common complex feline diseases at the Cornell University Hospital for Animals. Using a proprietary 340k single nucleotide polymorphism mapping array, we identified significant genome-wide associations with hyperthyroidism, diabetes mellitus, and eosinophilic keratoconjunctivitis. These results provide genomic locations for variant discovery and candidate gene screening for these important complex feline diseases, which are relevant not only to feline health, but also to the development of disease models for comparative studies.</p>
Other supporting data for our manuscript "Mapping the Single Cell Transcriptomic Response of Murine Diabetic Kidney Disease to Therapies"
<p>Other supplementary data for our paper "Mapping the Single Cell Transcriptomic Response of Murine Diabetic Kidney Disease to Therapies"</p>
A gene variation at the ZPR1 locus (rs964184) interacts with the type of diet to modulate postprandial triglycerides in patients with coronary artery disease: From the Cordioprev Study
<p>Background and Aims: rs964184 variant in the ZPR1 gene has been associated with blood lipids levels both in fasting and postprandial state and with the risk of myocardial<br>infarction in high-risk cardiovascular patients. However, whether this association is modulated by diet has not been studied.</p> <p>Objective: To investigate whether the type of diet (low-fat or Mediterranean diets) interacts with genetic variability at this loci to modulate fasting and postprandial lipids in<br>coronary patients.</p> <p>Materials and Methods: The genotype of the rs964184 polymorphism was determined in the Cordioprev Study population (NCT00924937). Fasting and Postprandial triglycerides were assessed before and after 3 years of dietary intervention with either a Mediterranean or a low-fat diet. Postprandial lipid assessment was done by a 4-h oral fat tolerance test (OFTT). Differences in triglycerides levels were identified using repeated-measures ANCOVA.</p> <p>Results: From 523 patients (85% males, mean age 59 years) that completed the OFTT at baseline and after 3 years of intervention and had complete genotype information, 125<br>of them were carriers of the risk allele G. At the start of the study, these patients showed a higher fasting and postprandial triglycerides (TG) plasma levels. After 3 years of dietary<br>intervention, G-carriers following a Mediterranean Diet maintained higher fasting and postprandial triglycerides, while those on the low-fat diet reduced their postprandial<br>triglycerides to similar values to the population without the G-allele.</p> <p>Conclusion: After 3 years of dietary intervention, the altered postprandial triglyceride response induced by genetic variability in the rs964184 polymorphism of the ZPR1 gene<br>can be modulated by a low-fat diet, better than by a Mediterranean diet, in patients with coronary artery disease.</p>
An open-access database of infectious disease transmission trees to explore superspreader epidemiology
Historically, emerging and reemerging infectious diseases have caused large, deadly, and expensive multinational outbreaks. Often outbreak investigations aim to identify who infected whom by reconstructing the outbreak transmission tree, which visualizes transmission between individuals as a network with nodes representing individuals and branches representing transmission from person to person. We compiled a database, called OutbreakTrees, of 382 published, standardized transmission trees consisting of 16 directly transmitted diseases ranging in size from 2 to 286 cases. For each tree and disease, we calculated several key statistics, such as tree size, average number of secondary infections, the dispersion parameter, and the proportion of cases considered superspreaders, and examined how these statistics varied over the course of each outbreak and under different assumptions about the completeness of outbreak investigations. We demonstrated the potential utility of the database through 2 short analyses addressing questions about superspreader epidemiology for a variety of diseases, including Coronavirus Disease 2019 (COVID-19). First, we found that our transmission trees were consistent with theory predicting that intermediate dispersion parameters give rise to the highest proportion of cases causing superspreading events. Additionally, we investigated patterns in how superspreaders are infected. Across trees with more than 1 superspreader, we found preliminary support for the theory that superspreaders generate other superspreaders. In sum, our findings put the role of superspreading in COVID-19 transmission in perspective with that of other diseases and suggest an approach to further research regarding the generation of superspreaders. These data have been made openly available to encourage reuse and further scientific inquiry.
Data and code from: Mixed infection, risk projection and misdirection: Interactions among pathogens alter links between host resources and disease
<p>A growing body of literature links resources of hosts to their risk of infectious disease. Yet most hosts encounter multiple pathogens, and projections of disease risk based on resource availability could be fundamentally wrong if they do not account for interactions among pathogens within hosts. Here, we measured infection risk of grass hosts (<i>Avena sativa</i>) exposed to three naturally-co-occurring viruses either singly or jointly (barley and cereal yellow dwarf viruses [B/CYDVs]: CYDV-RPV, BYDV-PAV, and BYDV-SGV) along experimental gradients of nitrogen and phosphorus supply. We asked whether disease risk (i.e., infection prevalence) differed in single versus co-inoculations, and whether these differences varied with rates and ratios of nitrogen and phosphorus supply. In single inoculations, the viruses did not respond strongly to nitrogen or phosphorus. However, in co-inoculations, we detected illustrative cases of 1) resource-dependent antagonism (RPV with increasing N; possibly due to competition), 2) resource-dependent facilitation (SGV with decreasing N:P; possibly due to immunosuppression), and 3) weak or no interactions within hosts (for PAV). Together, these within-host interactions created emergent patterns for co-inoculated hosts, with both infection prevalence and viral richness increasing with the combination of low nitrogen and high phosphorus supply. We demonstrate that knowledge of multiple pathogens is essential for predicting disease risk from host resources, and that projections of risk that fail to acknowledge resource-dependent interactions within hosts could be qualitatively wrong. Expansions of theory from community ecology theory may help anticipate such relationships linking host resources to diverse pathogen communities.</p>
ScienceDex guides
Understand access before you commit
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.