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513 results for “prone”
Gene expression profile at single cell level of tissue- associated kidney NKp46+NK1.1+ or NK1.1+ ILC from healthy, nephritic and NKp46 blocking antibody treated NZB/W lupus prone mice
GEO Series GSE207139. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Gene expression in diabetes-prone (NZO/HiBomDife) and diabetes-resistant (C57BL/6.V-Lepob/ob) mouse strains
GEO Series GSE64956. Mus musculus. 6 samples. Type: Expression profiling by array.
Acute atopic dermatitis and urticaria imprints peripheral monocytes with proinflammatory-prone signature
GEO Series GSE256444. Homo sapiens. 1 samples. Type: Expression profiling by high throughput sequencing.
Follicular helper T cells express a metabolic and cell signaling gene signature in a lupus-prone murine model
GEO Series GSE157648. Mus musculus. 14 samples. Type: Expression profiling by high throughput sequencing.
Dataset from thesis entitled: Analysis of the relationship between the phylogeny and the spontaneous misfolding proneness of the prion protein across hundreds of species of the class Mammalia.
<p>This entry contains raw data from the PhD thesis entitled "Analysis of the relationship between the phylogeny and the spontaneous misfolding proneness of the prion protein across hundreds of species of the class Mammalia." presented by Cristina Sampedro Torres-Quevedo in july 2024 at the University of the Basque Country (UPV/EHU). </p> <p>Among these raw data we include the alignment of 876 recombinant prion protein sequences from mammalian species, the phylogenetic tree that resulted from this alignment and PrPDex files that summarize the information obtained for many of the proteins included in the thesis (also available at prpdex.com). </p> <p>Abstract from the thesis: </p> <p>Transmissible spongiform encephalopathies (TSEs) or prion diseases are a group of invariably fatal neurodegenerative diseases that affect a range of mammalian species, including humans. These diseases are caused by the misfolding of the cellular prion protein (PrP<sup>C</sup>) into a toxic, aggregation-prone isoform (PrP<sup>Sc</sup>, from scrapie, the first identified prion disease). Despite this misfolding being the primary pathogenic event, the molecular mechanisms underlying this process remain largely unknown.</p> <p>The prion protein is highly conserved across species. However, despite the similarity between the amino acid sequences of the prion protein (PrP) among mammals, some species present much lower susceptibility to prion diseases. The key to this behaviour likely lays on the enhanced resistance of these animal species’ prion proteins to acquire a <em>bona fide</em> prion conformation. It is, therefore, conceivable that the tertiary structure and interspecific variations, ultimately encoded in the primary structure, determine the proneness of a PrP to misfolding. For this reason, the differences in the PrP sequence between mammalian species were systematically analysed to study the <em>PRNP</em> gene from a phylogenetic perspective, potentially unveiling evolutionary events related to prion diseases.</p> <p>A comprehensive database of hundreds of mammalian PrP sequences, the largest collection gathered so far, was generated, and phylogenetic trees were constructed based on nucleotide sequence variations. To this aim, 876 prion protein genetic sequences (from codon 90 to codon 231 approximately) from over 600 different mammalian species were aligned and a <em>PRNP</em> gene-based phylogenetic tree was built.</p> <p>Classical phylogenetic orders, classified according to multigenic analyses, tend to maintain their clusterization when using the <em>PRNP</em> gene as a readout of phylogenetic similarity. Nonetheless, the few differences found may shed some light on potential evolutionary constraints posed by prion disorders. Moreover, this phylogenetic study was combined with an <em>in vitro</em> misfolding study. The recently developed Protein Misfolding Shaking Amplification (PMSA), which allows to generate <em>bona fide</em> prions spontaneously, was used to evaluate the tendency of many of these proteins to misfold. This comprehensive analysis spanned a wide range of mammalian prion protein sequences. <span> </span></p> <p>This study has allowed to assign a numerical misfolding proneness score to each protein variant studied, ranking them based on their capacity to misfold spontaneously. Furthermore, this study presents data, on top of the tendency to misfold, on predicted protein stability, <em>in vitro </em>propagation, and <em>in vivo</em> infectious capabilities, whenever known. It also includes phylogenetic information about the species and lists of species with identical sequences.</p> <p>Both the phylogeny and misfolding studies have given rise to a large volume of data that may allow to determine the effect of distinct amino acids at each polymorphic position of the PrP on misfolding. This extremely complex phenomenon, influenced by multiple residues and the overall amino acidic context, will be the basis for future studies. These studies may require more sophisticated computational analyses or machine learning approaches than the visual analysis performed for this work. Nevertheless, our approach of coupling the phylogenetic information of the <em>PRNP</em> gene tree with misfolding capacity assessment has allowed us to conclude, among others, that prion diseases have not posed a constraint on the evolution of the <em>PRNP</em> gene. There are no clusters of phylogenetically distant species grouped by distinct prion-disease-resistant mutations. Moreover, the misfolding propensity does not correlate with general sequence similarity to the gold standard, the so-called universal prion acceptor, bank vole prion protein, nor with the predicted stability of the globular form of each PrP. In addition, from a more practical perspective, the resources and the wealth of data generated offer abundant models for structural and pathobiological studies. Among these, we can highlight designing new substrates for ultrasensitive prion detection methods, developing animal models with enhanced susceptibility to speed up preclinical studies, or designing dominant negative proteins for therapeutic applications.</p>
Fluid Responsiveness in Prone Patients
ClinicalTrials.gov study NCT06254456. IPD Sharing: NO. Countries: 0. Publications: 0.
Adult-specific trimethylation of histone H3 lysine 4 is prone to dynamic changes with aging in C. elegans somatic cells
GEO Series GSE101964. Caenorhabditis elegans. 28 samples. Type: Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other.
Acute atopic dermatitis and urticaria imprints peripheral monocytes with proinflammatory-prone signature
GEO Series GSE255396. Homo sapiens. 10 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Gene expression profile of the major phenotypic subsets of tissue-resident and tissue disease-associated macrophages from healthy and nephritic NZB/W lupus prone mice respectively in comparison to dis
GEO Series GSE269402. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Dynamic cerebrovascular autoregulation in patients prone to postural syncope: Comparison of techniques assessing the autoregulation index from spontaneous variability series
<p>Gelpi F, Bari V, Cairo B, De Maria B, Tonon D, Rossato G, Faes L, Porta A. Dynamic cerebrovascular autoregulation in patients prone to postural syncope: Comparison of techniques assessing the autoregulation index from spontaneous variability series. Auton Neurosci. 2022 Jan;237:102920. doi: 10.1016/j.autneu.2021.102920. Epub 2021 Nov 18. PMID: 34808528.</p> <p>Abstract</p> <p>Three approaches to the assessment of cerebrovascular autoregulation (CA) via the computation of the autoregulation index (ARI) from spontaneous variability of mean arterial pressure (MAP) and mean cerebral blood flow velocity (MCBFV) were applied: 1) a time domain method (TDM); 2) a nonparametric method (nonPM); 3) a parametric method (PM). Performances were tested over matched and surrogate unmatched pairs. Data were analyzed at supine resting (REST) and during the early phase of 60° head-up tilt (TILT) in 13 subjects with previous history of postural syncope (SYNC, age: 28 ± 9 yrs.; 5 males) and 13 control individuals (noSYNC, age: 27 ± 8 yrs.; 5 males). Analysis was completed by computing autonomic markers from heart period (HP) and systolic arterial pressure (SAP) variability series via spectral approach. HP and SAP spectral indexes suggested that noSYNC and SYNC groups exhibited different autonomic responses to TILT. ARI analysis indicated that: i) all methods have a sufficient statistical power to separate matched from unmatched pairs with the exception of nonPM applied to impulse response; ii) ARI estimates derived from different methods might be uncorrelated and, even when correlated, might exhibit a significant bias; iii) orthostatic stressor did not induce any evident ARI change in either noSYNC or SYNC individuals; iv) this conclusion held regardless of the method. Methods for the ARI estimation from spontaneous variability provide different ARIs but none indicate that noSYNC and SYNC subjects have different dynamic component of CA.</p>
Integrated N-mixture models generally perform well against other models for false positive prone data in ecological applications
Open the record for dataset details and reuse information.
Spectral decomposition of cerebrovascular and cardiovascular interactions in patients prone to postural syncope and healthy controls.
<p>Pernice R, Sparacino L, Bari V, Gelpi F, Cairo B, Mijatovic G, Antonacci Y, Tonon D, Rossato G, Javorka M, Porta A, Faes L. Spectral decomposition of cerebrovascular and cardiovascular interactions in patients prone to postural syncope and healthy controls. Auton Neurosci. 2022 Nov;242:103021. doi: 10.1016/j.autneu.2022.103021. Epub 2022 Aug 9. PMID: 35985253.</p> <p>Abstract</p> <p>We present a framework for the linear parametric analysis of pairwise interactions in bivariate time series in the time and frequency domains, which allows the evaluation of total, causal and instantaneous interactions and connects time- and frequency-domain measures. The framework is applied to physiological time series to investigate the cerebrovascular regulation from the variability of mean cerebral blood flow velocity (CBFV) and mean arterial pressure (MAP), and the cardiovascular regulation from the variability of heart period (HP) and systolic arterial pressure (SAP). We analyze time series acquired at rest and during the early and late phase of head-up tilt in subjects developing orthostatic syncope in response to prolonged postural stress, and in healthy controls. The spectral measures of total, causal and instantaneous coupling between HP and SAP, and between MAP and CBFV, are averaged in the low-frequency band of the spectrum to focus on specific rhythms, and over all frequencies to get time-domain measures. The analysis of cardiovascular interactions indicates that postural stress induces baroreflex involvement, and its prolongation induces baroreflex dysregulation in syncope subjects. The analysis of cerebrovascular interactions indicates that the postural stress enhances the total coupling between MAP and CBFV, and challenges cerebral autoregulation in syncope subjects, while the strong sympathetic activation elicited by prolonged postural stress in healthy controls may determine an increased coupling from CBFV to MAP during late tilt. These results document that the combination of time-domain and spectral measures allows us to obtain an integrated view of cardiovascular and cerebrovascular regulation in healthy and diseased subjects.</p>
Fire-prone monodominant vegetation acts as carbon sinks after fire - Data
<p>These data are part of the analysis and results found in the article in process of publication entitled -</p> <p><strong>Fire-prone monodominant vegetation acts as carbon sinks after fire</strong></p>
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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.