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2,880 results for “variant”
Engineering an inhibitor resistant human CSF1R variant for microglia replacement [InVitro_RNA]
GEO Series GSE220213. Homo sapiens. 24 samples. Type: Expression profiling by high throughput sequencing.
Genotyping-By-Sequencing and Reference Genome Enabled Variant Discovery in Octoploid Strawberry
<p>(P0652) Genotyping-By-Sequencing and Reference Genome Enabled Variant Discovery in Octoploid Strawberry</p> <p>Genotyping-by-sequencing (GBS) approaches have enabled routine high-density genome-wide DNA variant discovery in numerous agriculturally important species. Applications of GBS in octoploid (2n = 8x = 56) strawberry (Fragaria × ananassa) have been hindered by the absence of a reference genome for physically mapping DNA sequences; for discovering variants with sub-genome resolution, or effectively distinguishing homologous from homeologous variation. High-quality reference genome assemblies have recently emerged, supplying the foundation for this study, which focused on demonstrating the utility of GBS for calling sub-genome specific DNA variants in octoploid strawberry. To reduce genomic DNA complexity, double-digest protocols were tested on diverse accessions with two restriction enzyme combinations (PstI-MseI and HindIII-MseI). GBS libraries were sequenced on an Illumina HiSeq 4000 using a 150 bp paired-end protocol. For the purpose of this study, we describe the deployment of a flexible bioinformatic pipeline for GBS-facilitated variant discovery in octoploid strawberry. The percentage of uniquely mapped reads ranged from 51.41% for PstI-MseI to 55.56% for HindIII- MseI resulting in 1,591,764 and 2,362,556 unique locations, respectively. The number of discovered variants was 2.5-fold greater for HindIII-MseI (491,811) than PstI-MseI (199,486). The GBS protocols uncovered a dense genome-wide landscape of DNA variants for high- precision genetic mapping, identification of DNA variants associated with agriculturally important phenotypes, genomic-enabled breeding, and other applications in octoploid strawberry.</p> <p>Poster: PDF of poster and abstract for PAG 2018 (P0652)</p> <p>Figures: PNGs of figures on the poster</p> <p>Scrips: Txt files of SLURM scripts used to generate the follow .vcf files.</p> <p>- 8x_GBS_0_index: Uses BWA to index the reference genome (Edger et al 2019) for later use.</p> <p>- 8x_GBS_1_Demultiplex: Used Sabre to demultiplex fastq.gz files. Demultiplex_key_PE links individuals to their unique barcode.</p> <p>- 8x_GBS_2_Main: adapter removal, sequence alignment, and individual variant calling as a SLURM array. results in a .gvcf file for individuals.</p> <p>- 8x_GBS_3_Variant: population-level variant calling to a final .vcf file</p> <p>VCF: Two VCF files from the two enzyme experiments. H = HindIII-MseI; P = PstI-MseI</p>
10XG CRAM files for "Characterization of large-scale structural variants using Linked-Reads" (Part 2 of 2)
<p>Here we propose novel algorithms to characterize large (>40 Kbp) interspersed segmental duplications, (> 80 Kbp) inversions, (> 100 Kbp) deletions, and (> 100 Kbp) translocations using Linked-Read sequencing data. Linked-Read sequencing provides long range information, where Illumina reads are tagged with barcodes that can be used to assign short reads to pools of larger (30-50 Kbp) molecules.</p> <p><br> Our methods rely on split molecule sequence signature that we have previously described. Similar to the split read, split molecules refer to large segments of DNA that span an SV breakpoint. Therefore, when mapped to the reference genome, the mapping of these segments would be discontinuous.</p> <p><br> We redesign our earlier algorithm, VALOR, to specifically leverage Linked-Read sequencing data to discover large <br> structural variation. We implement our new algorithms in a new software package, called VALOR2. </p>
Raw diffraction data for [NiFeSe] hydrogenase G491A variant pressurized with Kr gas - dataset G491A-Kr
<p>Diffraction data measured at ESRF beamline ID30A-3 on September 27, 2017.</p>
Data from: Krabbe disease variant classification using parental blood-based diagnostic RNA-seq
<p>Krabbe disease (KD) is a rare autosomal recessive lysosomal storage disorder (LSD) associated with severe neurodegeneration and high mortality and is one of most prevalent LSDs at a recent estimate of 1 in 12,080 live births. The disease pathogenesis is related to low/undetectable galactocerebrosidase (GALC) activity resulting in an accumulation of a cytotoxic GALC substrate, psychosine (Psy), that leads to diffuse demyelination, psychomotor delays, and high morbidity/mortality across the disease spectrum. <span>Although</span> phenotypic prediction in newborns with a more common, homozygous 30kb deletion and very high Psy levels is straightforward, <u>there is a larger subset of patients identified through newborn screening with missense variants of uncertain significance (VUSs) that present with mildly elevated Psy levels that are difficult to interpret.</u> Functional data for a small set of missense variants support altered GALC trafficking and lysosomal localization in KD compared to a loss of catalytic function; however, there are >130 unclassified <i>GALC</i> VUSs (ClinVar; 73 missense) with no clear prognostic impact and differential onset. We are starting to performed blood-based diagnostic RNAseq (whole transcriptomics) to classify such VUSs. Here in this dataset, we performed blood-based diagnostic RNAseq on a couple to try to classify GALC gene variants in a family with Krabbe Disease (KD) and Phenylketonuria (PKU) clinical history. The single p.T513M variant carried by one of the couple was known to be pathogenic or likely pathogenic variant (ClinVar). Using RNAseq, we identified leaky splicing abnormality of portion of transcripts skipping of GALC exon 14 casuig a frameshift and a premature stop codon allowing us to confirm its classifciation as pathogenic. The single c.442+5G>A GALC variant carried by the other individual did not show any splicing defect suggesting this variant to be likely benign. This shows that blood-based targeted or whole mRNAseq can be perforemd for fater effieicnt diagnostis and varoant classification of GALC gene and confirmation of molecular diagnosis of KD. This dataset also shows that carrier individuals or parental RNAseq can be performed if children peripheral blood or dried blood spots (DBSs) are not available to diagnose and classify GALC variants. This type of usafe of clinical-grade functional omics platforms will enahance rare neurological disease diagnosis. </p>
Data from: Genome-wide association studies in dogs and humans identify ADAMTS20 as a risk variant for cleft lip and palate
Cleft lip with or without cleft palate (CL/P) is the most commonly occurring craniofacial birth defect. We provide insight into the genetic etiology of this birth defect by performing genome-wide association studies in two species: dogs and humans. In the dog, a genome-wide association study of 7 CL/P cases and 112 controls from the Nova Scotia Duck Tolling Retriever (NSDTR) breed identified a significantly associated region on canine chromosome 27 (unadjusted p=1.1 x 10-13; adjusted p= 2.2 x 10-3). Further analysis in NSDTR families and additional full sibling cases identified a 1.44 Mb homozygous haplotype (chromosome 27: 9.29 – 10.73 Mb) segregating with a more complex phenotype of cleft lip, cleft palate, and syndactyly (CLPS) in 13 cases. Whole-genome sequencing of 3 CLPS cases and 4 controls at 15X coverage led to the discovery of a frameshift mutation within ADAMTS20 (c.1360_1361delAA (p.Lys453Ilefs*3)), which segregated concordant with the phenotype. In a parallel study in humans, a family-based association analysis (DFAM) of 125 CL/P cases, 420 unaffected relatives, and 392 controls from a Guatemalan cohort, identified a suggestive association (rs10785430; p =2.67 x 10-6) with the same gene, ADAMTS20. Sequencing of cases from the Guatemalan cohort was unable to identify a causative mutation within the coding region of ADAMTS20, but four coding variants were found in additional cases of CL/P. In summary, this study provides genetic evidence for a role of ADAMTS20 in CL/P development in dogs and as a candidate gene for CL/P development in humans.
Data from: Multiple maize reference genomes impact the identification of variants by GWAS in a diverse inbred panel
Use of a single reference genome for genome-wide association studies (GWAS) limits the gene space represented to that of a single accession. This limitation can complicate identification and characterization of genes located within presence/absence variations (PAVs). In this study, we present the draft de novo genome assembly of PHJ89, an Oh43-type inbred line. Using three separate reference genome assemblies (B73, PH207, and PHJ89) that represent the predominant germplasm groups of maize, we generated three separate whole-seedling gene expression profile and single nucleotide polymorphism (SNP) matrices from a panel of 942 diverse inbred lines. We identified 34,447 (B73), 39,672 (PH207), and 37,436 (PHJ89) transcripts that are not present in the respective reference genome assembly. GWAS was conducted in the 942 inbred panel using both the SNP and expression data values to map sugarcane mosaic virus (SCMV) resistance. Highlighting the impact of alternative reference genomes in gene discovery, GWAS results for SCMV resistance using expression values as a surrogate measure of PAV resulted in robust detection of the physical location of a known resistance gene when using the B73 reference that contains the gene, but not when using the PH207 reference. This study provides the valuable resource of the Oh43-type PHJ89 genome assembly as well as SNP and expression data for 942 individuals generated using three different reference genomes.
Genetic characterisation of two novel heterozygous variants disrupting H bonds and 53 GPI gene variants
<p>55 Missense/nonsense mutations in the <i>GPI</i> gene.</p>
Structural variants in the HXB/BXH recombinant inbred panel
<p>Whole genome lined-read sequencing data of the HXB/BXH recombinant inbred panel was mapped using Longranger. Structural variants were merged using SURVIVOR.</p>
Location of Ryanodine Receptor Type 2 Associated Catecholaminergic Polymorphic Ventricular Tachycardia Variants Dataset
<h1>Location of RYR2 Associated CPVT Variants Dataset</h1> <p>Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited arrhythmia caused by pathogenic RYR2 variants. CPVT is characterized by exercise/stress-induced syncope and cardiac arrest in the absence of resting ECG and structural cardiac abnormalities.</p> <p>Here, we present a database collected from <strong>221</strong> clinical papers, published from 2001-October 2020, about CPVT associated RYR2 variants. <strong>1342</strong> patients, both with and without CPVT, with RYR2 variants are in the database. There are a total of <strong>964</strong> CPVT patients or suspected CPVT patients in the database. The database includes information regarding genetic diagnosis, location of the RYR2 variant(s), clinical history and presentation, and treatment strategies for each patient. Patients will have a varying depth of information in each of the provided fields.</p> <p>Database website: <a href="https://cpvtdb.port5000.com/">https://cpvtdb.port5000.com/</a></p> <h2>Dataset Information</h2> <p>This dataset includes:</p> <ol> <li>all_data.xlsx <ul> <li>Tabular version of the database</li> <li>Most relevant tables in the PostgreSQL database regarding patient sex, conditions, treatments, family history, and variant information were joined to create this database</li> <li>Views calculating the affected RYR2 exons, domains and subdomains have been joined to patient information</li> <li>m-n tables for patient's conditions and treatments have been converted to pivot tables - every condition and treatment that has at least 1 person with that condition or treatment is a column.</li> <li>NOTE: This was created using a LEFT JOIN of individuals and individual_variants tables. Individuals with more than 1 recorded variant will be listed on multiple rows. <ul> <li>There is only 1 patient in this database with multiple recorded variants (all intronic)</li> </ul> </li> </ul> </li> <li>20241219-dd040736b518.sql.gz<br> <ul> <li>PostgreSQL database dump</li> <li>Expands to about 200MB after loading the database dump</li> <li>The database includes two schemas: <ul> <li>public: Includes all information in patients and variants <ul> <li>Also includes all RYR2 variants in ClinVar</li> </ul> </li> <li>uta: Contains the rows from biocommons/uta database required to make the hgvs Python package validate RYR2 variants<br> <ul> <li>See <a href="https://github.com/biocommons/uta" target="_blank" rel="noopener">https://github.com/biocommons/uta</a> for more information</li> </ul> </li> </ul> </li> <li>NOTE: It is recommended to use this version of the database only for development or analysis purposes</li> </ul> </li> <li>database_tables.pdf <ul> <li>Contains information on most of the database tables and columns in the <code>public</code> schema</li> </ul> </li> <li>00_globals.sql <ul> <li>Required to load the PostgreSQL database dump</li> </ul> </li> </ol> <h2>How To Load Database Using Docker</h2> <p>First, download the `00_globals.sql` and `<DATE>_<ALEMBIC_REVISION>.gz.sql` file and move it into a directory. The default postgres image will load files from the `/docker-entrypoint-initdb.d` directory if the database is empty. See <a href="https://hub.docker.com/_/postgres#:~:text=and%20POSTGRES_DB.-,Initialization%20scripts,-If%20you%20would" target="_blank" rel="noopener">Docker Hub</a> for more information. Mount the directory with the files into the `/docker-entrypoint-initdb.d`.</p> <p>Example using docker compose with pgadmin and a volume to persist the data.</p> <pre><code># Use postgres/example user/password credentials volumes: mydatabasevolume: null services: db: image: postgres:16 restart: always environment: POSTGRES_PASSWORD: mysecretpassword POSTGRES_USER: postgres volumes: - '<INSERT LOCATION OF DIRECTORY WITH DATABASE DUMP HERE>:/docker-entrypoint-initdb.d/' - 'mydatabasevolume:/var/lib/postgresql/data'<br> ports:<br> - 5432:5432 pgadmin: image: dpage/pgadmin4 environment: PGADMIN_DEFAULT_EMAIL: user@domain.com PGADMIN_DEFAULT_PASSWORD: SuperSecret<br> ports:<br> - 8080:80</code></pre> <h2>Analysis Code</h2> <p>See https://github.com/alexdaiii/cpvt_database_analysis for source code to create the xlsx file and analysis of the data.</p> <h2>Changelist</h2> <ul> <li>v0.3.0 <ul> <li>Removed inasscessable publications</li> <li>Updated publications tgo include information on what type of publication it is (e.g. Original Article, Abstract, Review, etc)</li> </ul> </li> <li> v0.2.1 <ul> <li>Updated all_patients.xlsx -> all_data.xlsx</li> <li>Corrected how the data from all the patient's conditions, diseases, treatments, and the patients' variants tables are joined</li> </ul> </li> </ul>
Clinical data for individuals from families with SLC32A1 variants
<div class="page"> <div class="section"> <div class="layoutArea"> <div class="column"> <p><strong>Objective:</strong> To identify the causative gene in a large unsolved family with genetic epilepsy with febrile seizures plus (GEFS+), we sequenced the genomes of family members, and then determined the contribution of the identified gene to the pathogenicity of epilepsies by examining sequencing data from 2772 additional patients.</p> <p><strong>Methods: </strong>We performed whole genome sequencing of three members of a GEFS+ family. Subsequently, whole exome sequencing (ES) data from 1165 epilepsy patients from the Epi4K dataset and 1329 Australian epilepsy patients from the Epi25 dataset was interrogated. Targeted resequencing was performed on 278 patients with FS or GEFS+ phenotypes. Variants were validated and familial segregation examined by Sanger sequencing.</p> <p><strong>Results:</strong> Eight previously unreported missense variants were identified in SLC32A1, coding for the vesicular inhibitory amino acid co-transporter VGAT. Two variants co- segregated with the phenotype in two large GEFS+ families containing eight and ten affected individuals, respectively. Six further variants were identified in smaller families with GEFS+ or idiopathic generalized epilepsy (IGE).</p> <p><strong>Conclusions:</strong> Missense variants in SLC32A1 cause GEFS+ and IGE. These variants are predicted to alter GABA transport into synaptic vesicles, leading to altered neuronal inhibition. Examination of further epilepsy cohorts will determine the full genotype-phenotype spectrum associated with SLC32A1 variants.</p> </div> </div> </div> </div>
Heterologous immunization with inactivated vaccine followed by mRNA booster elicits strong humoral and cellular immune responses against the SARS-CoV-2 Omicron variant
<p>The recent emergence of the Omicron variant has raised concerns on vaccine efficacy and the urgent need to study more efficient vaccination strategies. Here we evaluated the effect of an mRNA vaccine booster on immunogenicity in individuals vaccinated with two doses of inactivated vaccine. We observed that an mRNA vaccine booster significantly increased the plasma level of specific antibodies that bind to the receptor-binding domain (RBD) or the spike (S) ectodomain (S1+S2) of both the G614 and the Omicron variants, compared to two doses of homologous inactivated vaccine. The level of RBD- and S-specific IgG antibodies and virus neutralization titers against variants of concern in the heterologous vaccination group were similar to that in individuals receiving three doses of homologous mRNA vaccine or a boost of mRNA vaccine after infection, but markedly higher than that in individuals receiving three doses of a homologous inactivated vaccine. Moreover, this heterologous vaccination regime significantly enhanced the RBD-specific memory B cell response and S1-specific T cell response compared to two or three doses of homologous inactivated vaccine. Our study demonstrates that an mRNA vaccine booster in individuals vaccinated with inactivated vaccines can be highly beneficial, as it markedly increases the humoral and cellular immune responses against the virus, including the Omicron variant</p>
MiRLog and dbmiR: prioritization and functional annotation tools to study human microRNA sequence variants
<p>dbmiR is a comprehensive database for functional annotation of miRNA SNVs (Single Nucleotide Variants). It includes a precompiled list of all possible miRNA allelic SNVs, providing their biological annotations at nucleotide and miRNA levels. In dbmiR we also integrated MiRLog, a new meta-predictor we implemented to predict the functional effect of miRNA SNVs.</p> <p>dbmiR can be used only for non-commercial purposes because of the licenses associated with some of the included tools and databases.</p>
Germline variants in 5 LCLs, supplementary data
<p>These files are supplementary data for the article Laczik M, Erdős E, Ozgyin L, Hevessy Zs, Csősz É, Kalló G, Nagy T, Barta E, Póliska Sz, Szatmári I and Bálint BL: Extensive proteome and functional genomic profiling of variability between genetically identical human B-lymphoblastoid cells. The files (one in Variant Call Format, the other is the index of the former) are outputs from the GATK germline variant calling pipeline, summarizing all the variants found in five isogenic B-lymphoblastoid cell lines. For further details please see the article.</p>
scAllele variant calls and linkage events
<p>Variant calls (*.vcf.gz) and linkage events (*.mi_summary.tab) from</p> <p>- GM12878 cells</p> <p>- iPSC cells (individuals NA19098, NA19101, NA19239)</p> <p>- Lung cancer cells (individuals TH238 and TH179)</p>
Identification and single-base gene-editing functional validation of a cis-EPO variant as a genetic proxy for EPO-increasing therapies.
<p>Summary statistics for the genome-wide association study meta-analysis of circulating EPO in 6,127 individuals of European and African American descent. Effect sizes are aligned to allele 1. </p> <p>Description of column names:<br> # Marker - this is the marker name; chromosome:position<br> # Allele1 - the first allele for this marker in the first file where it occurs<br> # Allele2 - the second allele for this marker in the first file where it occurs<br> # Freq1 - weighted average of frequency for allele 1 across all studies<br> # FreqSE - corresponding standard error for allele frequency estimate<br> # MinFreq - minimum frequency for allele 1 across all studies<br> # MaxFreq - maximum frequency for allele 1 across all studies<br> # Effect - overall estimated effect size for allele1<br> # StdErr - overall standard error for effect size estimate<br> # P-value - meta-analysis p-value<br> # Direction - summary of effect direction for each study, with one '+' or '-' per study. Order of the studies is InCHIANTI, BLSA, HealthABC Europeans, PREVEND, HealthABC African Americans<br> # HetISq - I^2 statistic which measures heterogeneity on scale of 0-100%<br> # HetChiSq - chi-squared statistic in simple test of heterogeneity<br> # df - degrees of freedom for heterogeneity statistic<br> # HetPVal - P-value for heterogeneity statistic<br> # TotalSampleSize - overall sample size for that variant in the meta-analysis</p> <p> </p>
Identification and single-base gene-editing functional validation of a cis-EPO variant as a genetic proxy for EPO-increasing therapies.
<p>Raw fast-qc files for RNA sequencing analysis of whole <em>EPO</em> gene knock-outs generated through CRISPR-Cas9 gene-editing in HEK-293 cells compared to wild-type controls. </p> <p>Wild-type cell-lines (Empty 1 - Empty 4) were transfected with empty CRISPR-Cas9 constructs to ensure cells were treated under the same experimental conditions. Whole EPO gene knock-outs were generated using a double gRNA approach with CRISPR-Cas9 gene-targeting. Two whole EPO gene knock-out cell-lines were generated (KO-A and KO-B).</p> <p>Library preparation was performed using the TruSeq DNA HT Library Preparation Kit using the 3’ poly-A tail primer Oligo(dT) from Illumina (Illumina, California, USA). RNA Sequencing was performed using the Illumina HiSeq 2500 high-throughput sequencing system (Illumina, California, USA). We resulted in 75 bp paired-end sequences.</p> <p> </p>
Figure 5 from: Schmitt M, Uhl G (2017) Oulema septentrionis and O. erichsonii are neither conspecific nor melanic variants of O. melanopus as assessed by micro CT analysis of their lectotypes (Insecta, Coleoptera, Chrysomelidae, Criocerinae). In: Chaboo CS, Schmitt M (Eds) Research on Chrysomelidae 7. ZooKeys 720: 121-130. https://doi.org/10.3897/zookeys.720.19760
Figure 5 - Flagella of a Oulema duftschmidi b O. melanopus, photos taken at the same magnification.
Performance data for 10 DE variants on BBOB benchmark suite in 10 dimensions (1-12 problems)
Open the record for dataset details and reuse information.
Diversely evolved xibalbin variants from remipede venom inhibit 3 potassium channels and activate PKA-II and Erk1/2 signalling
<p><span><strong>Background:</strong> </span><span>The identification of novel toxins from overlooked and taxonomically exceptional species bears potential for various pharmacological applications. The remipede <em>Xibalbanus tulumensis</em>, an underwater cave-dwelling crustacean, is the only crustacean for which a venom system has been described. Its venom contains several xibalbin peptides that have an inhibitor cysteine knot (ICK) scaffold.</span></p> <p><strong><span>Result:</span></strong><span><strong> </strong>Our screenings revealed that all tested xibalbin variants particularly inhibit potassium channels. Xib<sub>1</sub> and xib<sub>13</sub>, with their eight-cysteine domain similar to spider knottins also inhibit voltage-gated sodium channels. No activity was noted on calcium channels. Expanding the functional testing we demonstrate that xib<sub>1</sub> and xib<sub>13</sub> increase PKA-II and Erk1/2 sensitization signaling in nociceptive neurons, which may initiate pain sensitization. Our phylogenetic analysis suggests that xib<sub>13</sub> either originates from the common ancestor of pancrustaceans or earlier while xib<sub>1</sub> is more restricted to remipedes. The ten-cysteine scaffolded xib<sub>2</sub> emerged from xib<sub>1</sub>, a result that is supported by our phylogenetic and machine learning-based analyses.</span></p> <p><strong><span>Conclusions</span></strong><span><strong>: </strong>Our functional characterization of synthesized variants of xib<sub>1</sub>, xib<sub>2</sub>, and xib<sub>13</sub> elucidates their potential as inhibitors of potassium channels in mammalian systems. The specific interaction of xib<sub>2</sub> with Kv1.6 channels, which are relevant to treating variants of epilepsy, shows potential for further studies. At higher concentrations, xib1 and xib13 activate the kinases PKA-II and ERK1/2 in mammalian sensory neurons, suggesting pain sensitization and potential applications related to pain research and therapy. While tested insect channels suggest that all probably act as neurotoxins, the biological function of xib<sub>1</sub>, xib<sub>2,</sub> and xib<sub>13</sub> requires further elucidation. A novel finding on their evolutionary origin is the apparent emergence of </span><em><span>X. tulumensis</span></em><span>-specific xib<sub>2</sub> from xib<sub>1</sub>. Our study is an important cornerstone for future studies to untangle the origin and function of these enigmatic proteins as important components of remipede but also other pancrustacean and arthropod venoms.</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.