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1,890 results for “Defects”
Research data for "Understanding Defects in Amorphous Silicon with Million-Atom Simulations and Machine Learning"
<p>This dataset contains structural data and ML local energies for the publication "Understanding Defects in Amorphous Silicon with Million-Atom Simulations and Machine Learning". Details of the contents can be found in README.txt. Code to analyse structures and reproduce figures from the publication are available at https://github.com/MorrowChem/understanding_defects</p>
Defective interferon signaling in the circulating monocytes of type 2 diabetic mice
<h1>Data Repository for scRNA-seq and Cell Communication Analysis in T2DM Stroke Model</h1> <p>This repository contains the data and Seurat/CellChat objects generated for analyzing the transcriptomic response of peripheral monocytes to Type 2 Diabetes Mellitus (T2DM) and ischemic stroke in a mouse model. Data were generated using single-cell RNA sequencing (scRNA-seq), bulk RNA-seq, and analysis with NicheNet and CellChat. This study aims to reveal molecular and cellular changes in diabetic and ischemic conditions, particularly focusing on interferon signaling and inflammation.</p> <h2>Repository Structure</h2> <h3>Root Files</h3> <ul> <li> <p><code>README.md</code>: This file, describing the repository and data files.</p> </li> <li> <p><code>cellchat_object/</code>: Contains RDA files for CellChat analysis.</p> </li> <li> <p><code>scrna_sequencing_raw/</code>: Raw scRNA-seq data files.</p> </li> <li> <p><code>seurat_object/</code>: Contains Seurat objects for clustering and visualization.</p> </li> <li> <p><code>trajectory_object/</code>: Contains Cell Data Set (CDS) objects for trajectory and pseudotime analysis.</p> </li> </ul> <h3>File Descriptions</h3> <h4><code>cellchat_object/</code></h4> <ul> <li> <p><strong>dbdb_case_cellchat.rda</strong>: CellChat object for the db/db mice with ischemic stroke. Analysis was conducted to identify cell-cell communication patterns altered due to stroke in diabetic conditions.</p> </li> <li> <p><strong>dbdb_control_cellchat.rda</strong>: CellChat object for db/db control (no stroke) mice. Provides baseline data for diabetic conditions.</p> </li> <li> <p><strong>dbp_case_cellchat.rda</strong>: CellChat object for the db/+ (normoglycemic) mice with ischemic stroke, representing the stroke model in non-diabetic conditions.</p> </li> <li> <p><strong>dbp_control_cellchat.rda</strong>: CellChat object for db/+ control (no stroke) mice. Baseline for non-diabetic, non-stroke conditions.</p> </li> </ul> <p><strong>Methods</strong>: CellChat analysis identifies ligand-receptor interactions to reveal cross-talk between monocyte subtypes, focusing on pathways affected by T2DM and stroke. These data provide insights into thromboinflammatory responses, interferon signaling, and immune suppression in diabetic mice.</p> <h4><code>scrna_sequencing_raw/</code></h4> <ul> <li> <p><strong>db_db-DMCAO.zip</strong>: Raw scRNA-seq data for db/db mice post-distal middle cerebral artery occlusion (DMCAO).</p> </li> <li> <p><strong>db_db-Sham.zip</strong>: Raw scRNA-seq data for db/db mice with sham surgery (control).</p> </li> <li> <p><strong>db_pos-Sham.zip</strong>: Raw scRNA-seq data for db/+ mice with sham surgery.</p> </li> <li> <p><strong>db_pos-dMCAO.zip</strong>: Raw scRNA-seq data for db/+ mice post-DMCAO.</p> </li> </ul> <p><strong>Methods</strong>: scRNA-seq was performed using 10X Genomics GemCode Technology. Data were processed with Cell Ranger (v1.3), and differential gene expression analysis was conducted in Seurat with normalization based on UMI counts.</p> <h4><code>seurat_object/</code></h4> <ul> <li> <p><strong>bloodstroke.rda</strong>: Seurat object containing processed scRNA-seq data of peripheral blood mononuclear cells (PBMCs) from both diabetic and normoglycemic mice under stroke and sham conditions. Contains cell clusters annotated using SingleR and the ImmGen database.</p> </li> <li> <p><strong>monocytes.rda</strong>: Seurat object specifically for monocytes, enriched through re-clustering in Seurat. Enables focused analysis of monocyte subsets and their responses to diabetic and ischemic conditions.</p> </li> </ul> <p><strong>Methods</strong>: Filtering was performed for cells with fewer than 500 detected genes, and data were normalized using log-normalization. Clustering was carried out with PCA and visualized with UMAP.</p> <h4><code>trajectory_object/</code></h4> <ul> <li> <p><strong>dbdb_control_cds.rda</strong>: Cell Data Set (CDS) object for db/db control monocytes, representing baseline differentiation trajectory under diabetic conditions.</p> </li> <li> <p><strong>dbdb_stroke_cds.rda</strong>: CDS for db/db stroke monocytes, used to observe pseudotime trajectories and differentiation in diabetic and ischemic states.</p> </li> <li> <p><strong>dbp_control_cds.rda</strong>: CDS for db/+ control monocytes, baseline data for normoglycemic mice.</p> </li> <li> <p><strong>dbp_stroke_cds.rda</strong>: CDS for db/+ stroke monocytes, tracking pseudotime trajectory in response to ischemic stroke.</p> </li> <li> <p><strong>monocytes_cds.rda</strong>: CDS focusing on monocyte trajectory across all experimental conditions, facilitating the comparison of diabetic and normoglycemic trajectories.</p> </li> </ul> <p><strong>Methods</strong>: Trajectory analysis was conducted in Monocle 3 to explore cellular differentiation paths. Trajectories reveal potential maturation stages and highlight changes due to T2DM and ischemic conditions.</p> <h2>Methodology Overview</h2> <ol> <li> <p><strong>scRNA-seq and Bulk RNA-seq</strong>: Mononuclear cells were isolated and sequenced using 10X Genomics protocols, with analysis in Seurat to determine cell clusters, particularly monocytes. Bulk RNA-seq was used for pathway validation in broader cell populations.</p> </li> <li> <p><strong>CellChat Analysis</strong>: Ligand-receptor interactions were identified in CellChat, analyzing how cell communication changes with T2DM and stroke. Pathways of interest include the Anxa1-Fpr2 axis for thromboinflammation and MHCII-CD4 for immune activation.</p> </li> <li> <p><strong>Trajectory Analysis</strong>: Using Monocle 3, we investigated monocyte differentiation paths to uncover the effects of T2DM and stroke on cellular progression. Results demonstrate disrupted monocyte differentiation and increased proinflammatory markers in diabetic stroke conditions.</p> </li> <li> <p><strong>NicheNet Analysis</strong>: Identified key ligands affecting monocyte gene expression in diabetic versus non-diabetic conditions, highlighting interferon signaling and inflammatory markers such as Ccl6, Ccl9, and Ifng.</p> </li> </ol> <h2>Notes</h2> <ul> <li> <p>Ensure all analyses respect data filtering thresholds as set in Seurat and Monocle.</p> </li> <li> <p>Refer to the manuscript for further details on experimental setup, animal models, and additional context.</p> </li> </ul> <h2>License</h2> <p>Data and scripts are available for non-commercial use under a Creative Commons License.</p>
Reconstruction of Full-Thickness Lower Eyelid Defects After BCC Excision Using a Modified Hughes Procedure
<p><strong><span>Background:</span></strong></p> <p><span>Basal cell carcinoma (BCC) is the most common malignant tumor of the eyelid</span><span>.</span><span> These cancers often necessitate eyelid reconstruction in ophthalmic plastic surgery, which poses significant challenges. This study describes the use of a tarsoconjunctival flap from the orbicularis oculi muscle of the upper eyelid for reconstructing full-thickness lower eyelid defects following BCC resection.</span></p> <p><span> </span></p> <p><strong><span>Methods:</span></strong></p> <p><span>Four consecutive patients with full-thickness lower eyelid BCC underwent radical resection with 3-mm margins, followed by reconstruction using a tarsoconjunctival flap from the upper eyelid. Digital photographs were taken at baseline and at 1, 3, and 6 months post-surgery to evaluate clinical outcomes. Histological examination confirmed complete tumor excision in all cases.</span></p> <p><span> </span></p> <p><strong><span>Results:</span></strong></p> <p><span>The modified Hughes procedure resulted in a high rate of functional and aesthetic success, with no recurrences observed over an average follow-up of 12 months. None of the patients experienced temporary forced eyelid closure, and both aesthetic and functional results were satisfactory.</span></p> <p><span> </span></p> <p><strong><span>Conclusions:<span> </span></span></strong></p> <p><span>The tarsoconjunctival flap from the upper eyelid is an effective method for reconstructing extensive full-thickness lower eyelid defects, providing excellent functional and aesthetic outcomes.</span></p>
Supplementary material from: Microfluidic vessel-on-chip platform for investigation of cellular defects in venous malformations and responses to various shear stress and flow conditions
Open the record for dataset details and reuse information.
Stim circuits for 'Accommodating Fabrication Defects on Floquet Codes with Minimal Hardware Requirements' manuscript
<p>Example Stim circuits for Honeycomb quantum memory experiments with defective qubits.</p> <p>Because accommodating each sample of fabrication defects requires a separate Stim circuit, we only provide example circuits rather than all Stim circuits used in simulations.</p> <p>Please note that the example circuits presented here are constructed by sampling defective qubits according to an iid distribution, with a single parameter defining the probability of an individual qubit being defective. In general a circuit which has a higher probability of each qubit being defective will perform worse than a circuit which has a lower probability of each qubit being defective. However, this does not necessarily mean that the specific circuits presented here will see that behaviour, as these are just individual samples from a large distribution.</p> <p>V2: Uploaded more example circuits with a higher target distance.</p>
Dataset for manuscript titled "Metal-like ductility and high hardness in nitrogen-rich HfN thin films by point defect superstructuring"
<p>Experimental data for support of claims in the paper. </p>
Dataset examples related to the publication entitled "High-Potential Test for Quality Control of Separator Defects in Battery Cell Production"
<p>Dataset examples and visualization program code for the publication entitled "High-Potential Test for Quality Control of Separator Defects in Battery Cell Production". Publication Doi: https://doi.org/10.3390/batteries7040064.</p>
Explanations for "Defect Identification, Categorization, and Repair: Better Together"
<p><strong>Explanations for "Defect Identification, Categorization, and Repair: Better Together"</strong></p>
Engineered nasal cartilage for the repair of osteoarthritic knee cartilage defects
<p>Data underlying the figures in the publication “Engineered nasal cartilage for the repair of osteoarthritic knee cartilage defects”, published in <em>Sci. Transl. Med., <strong>2021</strong>, 13, eaaz4499.</em></p> <p><a href="https://www.science.org/doi/10.1126/scitranslmed.aaz4499">https://www.science.org/doi/10.1126/scitranslmed.aaz4499</a></p> <p>Table of contents:</p> <p><strong>1. Data_file_S1</strong>: Experimental data for <em>Figures 2, 3, 6, Supplementary Figures S1-5 and Supplementary Tables 3-5</em>.</p> <p><strong>2. Table S1</strong>: Differentially expressed genes between nasal and articular chondrocytes. Fold change data was calculated with a positive log2 fold change (FC) indicating higher expression in nasal relative to articular chondrocytes. An adjusted (adj) P value < 0.05 was considered statistically significant.</p> <p><strong>3. Table S2</strong>: Pathway enrichment among differentially expressed genes (DEGs) between nasal and articular chondrocytes. Pathway enrichment was performed using the PANTHER (version 14.1) overrepresentation test based on the DEGs between nasal and articular chondrocytes (table S1). An FDR < 0.05 was considered statistically significant.</p>
Dataset related to article "Defective cyclophilin A induces TDP-43 proteinopathy: implications for amyotrophic lateral sclerosis and frontotemporal dementia"
<p>Dataset related to the article 10.1093/brain/awab333</p>
CREMI Defects
<p>Defect slices with annotations for data from https://cremi.org/.</p>
Validating x-ray line-profile defect analysis using atomistic models of deformed material
<p>Data and analysis (scripts and Jupyter notebooks) associated with publications:</p> <p>Validating x-ray line-profile defect analysis using atomistic models of deformed material (submitted to Physical Review Materials)</p> <p>Validation of x-ray line-profile analysis of extended defects in deformed crystals (submitted to Physical Review Letters)</p> <p>Preprints of these papers are included here</p>
Supplemental material for: Validation of intraluminal filling defect length to identify carotid free-floating thrombus in patients with stroke/TIA
<p><strong>Objective: </strong>To validate a previously proposed filling defect length threshold of >3.8 mm on CT-angiography (CTA) to discriminate between free-floating thrombus (FFT) and plaque of atheroma.</p> <p><b>Materials and Methods: </b>Prospective multicenter observational study of 100 participants presenting with TIA/stroke symptoms and a carotid intraluminal filling defect on initial CTA. Follow-up CTA was obtained within one week, and at weeks 2 and 4 if the intraluminal filling defect was unchanged in length. Resolution or decreased length was diagnostic of FFT, whereas its static appearance after 4 weeks was indicative of plaque. Diagnostic accuracy of FFT length was assessed by receiver operating characteristic analysis.</p> <p><b>Results: </b>Ninety-five participants (mean age [standard deviation], 68 [13] years; 61 men; 83 participants with FFT; 12 participants with a plaque) were evaluated. The >3.8 mm threshold had a sensitivity of 88% (73/83) (95% confidence interval {CI}: 78%, 94%) and specificity of 83% (10/12) (95% CI, 51%, 97%) (area under the curve [AUC], 0.91, p<.001) for the diagnosis of FFT. The optimal length threshold was >3.64 mm with a sensitivity of 89%( 74/83) (95% CI, 80%, 95%) and specificity of 83% (10/12) (95% CI, 51%, 97%). Adjusted logistic regression showed that every 1 mm increase in intraluminal filling defect length is associated with an increase in odds of FFT of 4.6 ([95% CI] 1.9-11.1; <i>p</i>=.01).</p> <p><b>Conclusion: </b>CTA enables accurate differentiation of FFT versus plaque using craniocaudal length thresholds.</p> <p><strong>Clinical Trial Identifier:</strong> <a href="http://www.clinicaltrials.gov">www.clinicaltrials.gov</a> NCT02405845.</p> <p><b>Classification of Evidence: </b>This study provides Class I evidence that in patients with TIA/stroke symptoms, the presence of a carotid intraluminal filling defect with length > 3.8 mm on CTA accurately discriminates free-floating thrombus from atheromatous plaque.</p>
Magnetic imaging with spin defects in hexagonal boron nitride
<p>Data relative to the publication arXiv:2207.10477</p>
Nonunique fraction of Fock exchange for defects in two-dimensional materials
<p>This dataset contains the input and output files for the defect calculations as described in the paper "Nonunique fraction of Fock exchange for defects in two-dimensional materials".</p> <ol> <li>ws2.tar.gz: PBE and PBE0, monolayer WS<sub>2</sub></li> <li>ws2_bulk.tar.gz: PBE and PBE0, bulk WS<sub>2</sub></li> <li>ws2_bgw.tar.gz: G<sub>0</sub>W<sub>0</sub>, monolayer WS<sub>2</sub></li> </ol> <p> </p>
Source Data for Xiao et al., Topological Superfluid Defects with Discrete Point Group Symmetries , Nature Communications 13, 4635 (2022).
<p>Source data for Figures 2-5. Source data for Supplementary Figures S2-S5 available upon request to David Hall (dshall@amherst.edu).</p>
Defect Identification, Categorization, and Repair:Better Together
<p><strong>CompDefect-replication-package</strong></p> <p><strong>This repository contains source code that we used to perform experiments in "Defect Identification, Categorization, and Repair: Better Together" paper.</strong></p> <p><strong>The paper is now under view.</strong></p> <p><strong><a href="https://arxiv.org/pdf/2204.04856.pdf">https://arxiv.org/pdf/2204.04856.pdf</a></strong></p>
Defect-induced tuning of polarity-dependent adsorption in hydrophobic–hydrophilic UiO-66
<p>Simulations outputs from DFT and MC calculations on UiO-66 structures</p>
Supplementary material for the publication: "Combining unsupervised and supervised learning in microscopy enables defect analysis of a full 4H-SiC wafer"
<p><span><span>This dataset contains postprocessed data for the publication „<span>Combining unsupervised and supervised learning in microscopy enables defect analysis of a full 4H-SiC wafer</span>“.</span></span></p>
Defective Zirconia Promotes Monometallic Iron Catalysts for Higher Alcohol Synthesis
<p>Datasets supporting the publication 'Defective Zirconia Promotes Monometallic Iron Catalysts for Higher Alcohol Synthesis'</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.