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4,540 results for “inflammation”
Pivotal Study to Assess the Efficacy, Safety and Tolerability of Dupilumab in Patients With Moderate-to-severe COPD With Type 2 Inflammation
ClinicalTrials.gov study NCT03930732. IPD Sharing: YES. Countries: 24. Publications: 5.
Inflammation and the Heart
ClinicalTrials.gov study NCT01589770. IPD Sharing: YES. Countries: 1. Publications: 1.
The Effect of Dupilumab on Lung Inflammation and Related Changes in Airway Volumes Detectable by Functional Respiratory Imaging in Patients With Moderate-severe Asthma
ClinicalTrials.gov study NCT04400318. IPD Sharing: YES. Countries: 13. Publications: 2.
Intracanalicular Dexamethasone Insert for Post-Corneal Cross-Linking Inflammation and Pain- The LINK Study
ClinicalTrials.gov study NCT04168112. IPD Sharing: NO. Countries: 1. Publications: 13.
Study of Relationship Between Vedolizumab Therapeutic Drug Monitoring, Biomarkers of Inflammation and Clinical Outcomes
ClinicalTrials.gov study NCT04567628. IPD Sharing: YES. Countries: 1. Publications: 1.
Aggravated Airway Inflammation: Research on Biological Treatment (Mepolizumab)
ClinicalTrials.gov study NCT04823585. IPD Sharing: NO. Countries: 1. Publications: 1.
Study to Evaluate the Effect of Secukinumab Compared to Placebo on Aortic Vascular Inflammation in Subjects With Moderate to Severe Plaque Psoriasis
ClinicalTrials.gov study NCT02690701. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
The Effectiveness of Brushing and Flossing Sequence on Control of Plaque and Gingival Inflammation
ClinicalTrials.gov study NCT03989427. IPD Sharing: YES. Countries: 1. Publications: 5.
Pivotal Study to Assess the Efficacy, Safety and Tolerability of Dupilumab in Patients With Moderate to Severe COPD With Type 2 Inflammation
ClinicalTrials.gov study NCT04456673. IPD Sharing: YES. Countries: 29. Publications: 2.
Differential effects of multiplex and uniplex affiliative relationships on biomarkers of inflammation
Open the record for dataset details and reuse information.
PI3Kg inhibition circumvents inflammation and mortality in SARS-CoV-2 and other infections
Open the record for dataset details and reuse information.
Multiplexed histology reveals phenotypic and spatial characteristics of human Innate Lymphoid Cells in chronic inflammation - Data tables
<p>Data tables containing image-based, single cell information for a tonsil and a colon data-set analyzed in CellProfiler: cell numbers, MFI of all markers, annotated cell types and cell allocations (X, Y coordinates).</p> <p> </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>
Data from: Effect of stretching on inflammation in a subcutaneous carrageenan mouse model analyzed at single-cell resolution
<p>Understanding the factors that influence the biological response to inflammation is crucial, due to its involvement in physiological and pathological processes, including tissue repair/healing, cancer, infections, and autoimmune diseases. We have previously demonstrated that in vivo stretching can reduce inflammation and increase local pro-resolving lipid mediators in rats, suggesting a direct mechanical effect on inflammation resolution. Here, we aimed to explore further the effects of stretching at the cellular/molecular level in a mouse subcutaneous carrageenan-inflammation model. Stretching for 10 minutes twice a day reduced inflammation, increased the production of pro-resolving mediator pathway intermediate 17-HDHA at 48h post carrageenan injection, and decreased both pro-resolving and pro-inflammatory mediators (e.g., PGE<sub>2</sub> and PGD<sub>2</sub>) at 96h. ScRNAseq analysis of inflammatory lesions at 96h showed that stretching increased the expression of both pro-inflammatory (<em>Nos2</em>) and pro-resolution (<em>Arg1</em>) genes in M1 and M2 macrophages at 96 hours. An intercellular communication analysis predicted specific ligand-receptor interactions orchestrated by neutrophils and M2a macrophages, suggesting a continuous neutrophil presence recruiting immune cells such as activated macrophages to contain the antigen while promoting resolution and preserving tissue homeostasis.</p>
Data from: A qualitative analysis of an Aβ-monomer model with inflammation processes for Alzheimer's disease
<p>We introduce and study a new model for the progression of Alzheimer's disease incorporating the interactions of Aβ-monomers, oligomers, microglial cells and interleukins with neurons through different mechanisms such as protein polymerization, inflammation processes and neural stress reactions. In order to understand the complete interactions between these elements, we study a spatially-homogeneous simplified model that allows to determine the effect of key parameters such as degradation rates in the asymptotic behavior of the system and the stability of equilibriums. We observe that inflammation appears to be a crucial factor in the initiation and progression of Alzheimer's disease through a phenomenon of hysteresis, which means that there exists a critical threshold of initial concentration of interleukins that determines if the disease persists or not in the long term. These results give perspectives on possible anti-inflammatory treatments that could be applied to mitigate the progression of Alzheimer's disease. We also present numerical simulations that allow to observe the effect of initial inflammation and concentration of monomers in our model.</p>
Supplemetary data for the paper "Knockdown of circular RNA hsa_circ_0003307 inhibits synovial inflammation in ankylosing spondylitis by regulating the PI3K/AKT pathway" by Yanyan Fang, Jian Liu*, Yan Long, Jianting Wen, Dan Huang, Ling Xin
<p>Statistical analyses and graphs were performed using Prism 8 software (GraphPad, La Jolla, USA). Age was analyzed using Student's t test (Supplementary Table 1A,B). Expression of circRNA_0003307 in PBMCs was analyzed using Welch's t-test (Supplementary Table 2A,B). CircRNA_0003307 expression in AS-FLS was analyzed using a one-way analysis of variance, then Games-Howell test (Supplementary Table 4A–C). The p-PI3K protein expression in AS-FLS was analyzed using a one-way analysis of variance, then Games-Howell test (Supplementary Table 5A–C). The p-AKT protein expression in AS-FLS was analyzed using a one-way analysis of variance, then Games-Howell test (Supplementary Table 6A–C). The TNF-α levels in AS-FLS was analyzed using a one-way analysis of variance, then Games-Howell test (Supplementary Table 7A–C). The TNFAIP2 levels in AS-FLS was analyzed using a one-way analysis of variance, then Games-Howell test (Supplementary Table 8A–C). Categorical variables were compared using chi-square test. Correlations were assessed using Spearman’s analysis because clinical characteristics were not normally distributed (Supplementary Table 3). A receiver operating characteristic (ROC) curve analysis was performed to judge whether circRNA_0003307 can be used as a diagnostic indicator for AS. P <0.05 indicates that the difference was statistically significant.</p>
Data for Human milk lactoferrin variation in relation to maternal inflammation and iron deficiency in northern Kenya
<p>This file contains the data utilized for a journal manuscript, "Human milk lactoferrin variation in relation to maternal inflammation and iron deficiency in northern Kenya" by Fujita, Wander, Paredes Ruvalcaba, and Odo, currently under review for publication. Data are found under the Data tab, and the variable coding information under the Code tab.</p> <p>Please contact Fujita (masakof@msu.edu) for questions regarding the data.</p> <p>In using the data, please cite the DOI for this file and the above-mentioned article. Also, please acknowledge the following parties for grant support:</p> <p> National Science Foundation (BCS-0622358, BCS-1638167);</p> <p> Wenner-Gren Foundation (Gr. 7460, Gr. 9278);</p> <p> African Futures Research Leadership Program of the Alliances for African Partnership, Michigan State University; and</p> <p> Provost Undergraduate Research Initiative Grant, Michigan State University </p> <p>The data originates in the 2006 fieldwork among the Ariaal people in northern Kenya under approvals by the institutional review boards of the University of Washington and Kenya Medical Research Institute. The lactoferrin concentration in milk was determined more recently using de-identified milk specimens, and as such required no further approvals.</p> <p> </p>
Psoriatic arthritis disease subtypes are phenocopied in a novel humanized murine model of psoriasis and joint inflammation
<p><em><span>Data processing and analysis</span></em></p> <p><span>Data normalization, quality control, and analysis was conducted by the UPMC Hillman Cancer Bioinformatics Services. Following the GeoMX NGS pipeline (<span>sequencing saturation 92%±0.12% (mean±S.E.M)), t</span>he resulting read count matrix was passed through robust QC procedure to remove ROIs of low surface area (<5000 µm<sup>2</sup>) or low perfect aligned reads (<80%), and probes of low quality or identified as global or local outliers (fails Grubbs outlier test in ≥ 20% segments). The remaining data were back-ground subtracted and Q3 normalized to house-keeping genes. ROIs were considered positive for CD8 T cells if their CD8 memory T cell deconvolution fraction was > 0 (R, spatialDecon, CellProfileLibrary; Human Adult ImmuneTumor_safeTME profile). Genes differentially expressed between groups of interest were detected using gene-wise linear modeling in R (edgeR, limma v3.50.3), with p-value adjusted for false discovery rate. Contrasts of groups were performed using t-tests at a significance level of 0.05.</span></p>
Designer high-density lipoprotein particles enhance endothelial barrier function and suppress inflammation
<p>High-density lipoprotein (HDL) nanoparticles promote endothelial cell (EC) function and suppress inflammation, but their utility in treating EC dysfunction has not been fully explored. Here, we describe a fusion protein named ApoA1-ApoM (A1M) consisting of apolipoprotein A1 (ApoA1), the principal structural protein of HDL that forms lipid nanoparticles, and ApoM, a chaperone for the bioactive lipid sphingosine 1-phosphate (S1P). A1M forms HDL-like particles, binds S1P, and is signaling competent. Molecular dynamic simulations showed that the S1P-bound ApoM moiety in A1M efficiently activated the EC surface receptors. Treatment of human umbilical vein endothelial cells (HUVECs) with A1M-S1P stimulated barrier function either alone or cooperatively with other barrier-enhancing molecules, including the stable prostacyclin analog iloprost, and suppressed cytokine-induced inflammation. A1M-S1P injection into mice during sterile inflammation suppressed neutrophil influx and inflammatory mediator secretion. Moreover, systemic A1M administration led to a sustained increase in circulating HDL-bound S1P and suppressed inflammation in a murine model of LPS-induced endotoxemia. We propose that A1M administration may enhance vascular endothelial barrier function, suppress cytokine storm, and promote resilience of the vascular endothelium.</p>
Systemic inflammation accelerates neurodegeneration in a rat model of Parkinson's disease overexpressing human alpha synuclein
<p><span>Parkinson’s disease (PD) involves genetic and<span> </span>environmental risk factors. Increasing research efforts have been made to understand how they interact<span> </span>to<span> </span>impair<span> </span>homeostasis<span> </span>and<span> </span>elevate<span> </span>risk. Inflammation could be one unifying factor. In this study, <em>wild-type</em> (WT) and overexpressing human </span><span>α</span><span>-synuclein (<em>Snca</em><sup>+/+</sup>) rats <span>were intraperitoneally injected with a single dose of </span>lipopolysaccharide<span> </span>(LPS) or with saline (SAL). In these animals we assessed </span><span>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 <em>Snca<sup>+/+</sup> </em>rats triggered long-lasting increased activation of pro-inflammatory microglial markers, infiltrating monocytes and T-lymphocytes. However, only LPS <em>Snca</em><sup>+/+</sup> rats displayed dopaminergic neuronal loss in the <em>substantia<span> </span>nigra pars compacta<span> </span></em>(SNpc), associated with a reduction of evoked dopamine<span> release </span>in the striatum. No significant<span> </span>changes were observed in the behavioral domain. </span></p> <p><span> </span></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.