Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
11,745
datasets available to search
ShareScore release 0.9.0
Dataset results
11,745 results for “Disorder”
Remodeling dental anatomy vs sham therapy for chronic temporomandibular disorders: A placebo-controlled randomized clinical trial
Open the record for dataset details and reuse information.
Data from: Common gray and white matter abnormalities in schizophrenia and bipolar disorder
This study aimed to investigate abnormalities in the gray matter and white matter (GM and WM, respectively) that are shared between schizophrenia (SZ) and bipolar disorder (BD). We used 3T-magnetic resonance imaging to examine patients with SZ, BD, or healthy control (HC) subjects (aged 20-50 years, N = 65 in each group). We generated modulated GM maps through voxel-based morphometry (VBM) for T1-weighted images and skeletonized fractional anisotropy, mean diffusion, and radial diffusivity maps through tract-based special statistics (TBSS) methods for diffusion tensor imaging (DTI) data. These data were analyzed using a generalized linear model with pairwise comparisons between groups with a family-wise error corrected P < 0.017. The VBM analysis revealed widespread decreases in GM volume in SZ compared to HC, but patients with BD showed GM volume deficits limited to the right thalamus and left insular lobe. The TBSS analysis showed alterations of DTI parameters in widespread WM tracts both in SZ and BD patients compared to HC. The two disorders had WM alterations in the corpus callosum, superior longitudinal fasciculus, internal capsule, external capsule, posterior thalamic radiation, and fornix. However, we observed no differences in GM volume or WM integrity between SZ and BD. The study results suggest that GM volume deficits in the thalamus and insular lobe along with widespread disruptions of WM integrity might be the common neural mechanisms underlying the pathologies of SZ and BD.
Experimental Tuning of Transport Regimes in Hyperuniform Disordered Photonic Materials
<p>This repository contains the videos related to the paper entitled "Experimental Tuning of Transport Regimes in Hyperuniform Disordered Photonic Materials" published in <a href="https://doi.org/10.1103/PhysRevLett.125.127402"><em>Physical Review Letters</em> <strong>125</strong>, 127402 (2020)</a>. They show how the how the electromagnetic wave propagates in the cavity for different frequency ranges.</p> <ul> <li>video-1-stealth.mp4: Stealth regime (Gaussian bandpass filter, <span class="math-tex">\(f_0 = 1.75\ \mathrm{GHz}\)</span>, <span class="math-tex">\(\Delta \nu = 0.25\ \mathrm{GHz}\)</span>)</li> <li>video-2-stealth.mp4: Stealth regime (Gaussian bandpass filter, <span class="math-tex">\(f_0 = 2.25\ \mathrm{GHz}\)</span>, <span class="math-tex">\(\Delta \nu = 0.25\ \mathrm{GHz}\)</span>)</li> <li>video-3-diffusion.mp4: Wave diffusion (Gaussian bandpass filter, <span class="math-tex">\(f_0 = 3.50\ \mathrm{GHz}\)</span>, <span class="math-tex">\(\Delta \nu = 0.25\ \mathrm{GHz}\)</span>)</li> <li>video-4-localizationBelowGap.mp4: Dielectric Anderson localized modes just below the bandgap (Gaussian bandpass filter, <span class="math-tex">\(\Delta \nu = 0.25\ \mathrm{GHz}\)</span>)</li> <li>video-5-bandgap.mp4: Square filter in the bandgaps</li> <li>video-6-localizationAboveGap.mp4: Air Anderson localized modes just above the bandgap (Gaussian bandpass filter, <span class="math-tex">\(\Delta \nu = 0.25\ \mathrm{GHz}\)</span>)</li> <li>video-7-diffusion.mp4: Wave diffusion (Gaussian bandpass filter, <span class="math-tex">\(f_0 = 6.50\ \mathrm{GHz}\)</span>, <span class="math-tex">\(\Delta \nu = 0.25\ \mathrm{GHz}\)</span>)</li> </ul>
Three dimensional dataset combining gait and full body movement of children with autism spectrum disorders collected by Kinect v2 camera
<p><span>To the best of our knowledge, this is the maiden attempt to build a three-dimensional dataset that combines gait and body movement analysis of children with Autism Spectrum Disorders (ASD) in controlled environments for fifty children with autism children and fifty typical children. A 3D dataset includes 3D joints positions, the corresponding skeleton movement video, joints trajectories video captured by Kinect v2, and color videos captured by Samsung Note 9 rear camera. On the other hand, color videos for 9 children suffer from severe autism is also included for scientific benefit. Finally, the dataset includes 700 folders (350 for typical children, 350 for children with ASD) which include 3D files of tracked joints, angles between joints, and skeleton tracking video related to the augmentation of the original dataset based on seven transformations described in the paper.</span></p>
data set related to article Brain Network Organization Correlates with Autistic Features in Preschoolers with Autism Spectrum Disorders and in Their Fathers - Preliminary Data from a DWI Analysis
<p>This record contains raw data related to article Brain Network Organization Correlates with Autistic Features in Preschoolers with Autism Spectrum Disorders and in Their Fathers - Preliminary Data from a DWI Analysis</p>
data set related to article Effect of melatonin in children with attention deficit/ hyperactivity disorder wih anorexia nervosa restricting type
<p>This record contains raw data related to article Effect of melatonin in children with attention deficit/ hyperactivity disorder wih anorexia nervosa restricting type</p>
Data from: Severe childhood speech disorder: Gene discovery highlights transcriptional dysregulation
<p><b><span>Objective:</span></b><span> Determining the genetic basis of speech disorders provides insight into the neurobiology of human communication. Despite intensive investigation over the past two decades, the etiology of most children with speech disorder remains unexplained. Here we </span>searched for a genetic etiology in children with severe speech disorder, specifically childhood apraxia of speech (CAS).</p> <p><b>Methods:</b> Precise phenotyping together with research genome or exome analysis were performed on children referred with a primary diagnosis of CAS, as well as other medical or neurodevelopmental co-morbidities. Gene co-expression and gene set enrichment analyses analyses were conducted on high confidence gene candidates.</p> <p><b>Results:</b> 34 probands ascertained for CAS were studied. In 11/34 (32%) probands, we identified highly plausible pathogenic single nucleotide (n=10, <i>CDK13, EBF3, GNAO1, GNB1, DDX3X, MEIS2, POGZ, SETBP1, UPF2, ZNF142</i>) or copy number (n = 1, 5q14.3q21.1 locus) variants in novel genes or loci for CAS. Testing of parental DNA was available for nine probands and confirmed that the variants had arisen <i>de novo</i>. Eight genes encode proteins critical for regulation of gene transcription, and analyses of transcriptomic data found CAS-implicated genes were highly co-expressed in the developing human brain.</p> <p><b>Conclusion:</b><i> </i>We identify the likely genetic aetiology in 11 patients with CAS and implicate 9 genes for the first time. We find that CAS is often a sporadic monogenic disorder, and highly genetically heterogeneous. Highly penetrant variants implicate shared pathways in broad transcriptional regulation, highlighting the key role of transcriptional regulation in normal speech development. CAS is a distinctive, socially debilitating clinical disorder, and understanding its molecular basis is the first step towards identifying precision medicine approaches.</p>
Data from: Sleep, major depressive disorder and Alzheimer's disease: a Mendelian randomisation study
<div class="WordSection1"> <span><span>Objective</span></span> <p><span>To explore the causal relationships between sleep, major depressive disorder (MDD), and Alzheimer's disease (AD).</span></p> <span><span>Methods</span></span> <p><span>We conducted bi-directional two-sample Mendelian randomisation analyses. Genetic associations were obtained from the largest genome-wide association studies currently available in UK Biobank (N=446,118), the Psychiatric Genomics Consortium (N=18,759), and the International Genomics of Alzheimer's Project (N=63,926). We used the inverse variance weighted Mendelian randomisation method to estimate the causal effects, and the weighted median and MR-Egger for sensitivity analyses to test for pleiotropic effects. </span></p> <span><span>Results</span></span> <p><span>We found that higher risk of AD was significantly associated with being a "morning person" (odds ratio (OR)=1.01, P=0.001), shorter sleep duration (self-reported: β=-0.006, P=1.9×10<sup>-4</sup>; accelerometer-based: β=-0.015, P=6.9×10<sup>-5</sup>), less likely to report long sleep (β=-0.003, P=7.3×10<sup>-7</sup>), earlier timing of the least active 5 hours (β=-0.024, P=1.7×10<sup>-13</sup>), and a smaller number of sleep episodes (β=-0.025, P=5.7×10<sup>-14</sup>) after adjusting for multiple comparisons. We also found that higher risk of AD was associated with lower risk of insomnia (OR=0.99, P=7×10<sup>-13</sup>). However, we did not find evidence that these abnormal sleep patterns were causally related to AD or a significant causal relationship between MDD and risk of AD. </span></p> <span><span>Conclusion</span></span> <p><span>We found that AD may causally influence sleep patterns. However, we did not find evidence supporting a causal role of disturbed sleep patterns in AD or evidence for a causal relationship between MDD and AD risk.</span></p> </div> <p> </p>
Static Disorder in Excitation Energies of the Fenna-Matthews-Olson Protein: Structure-Based Theory Meets Experiment
<p>The files contain atomic coordinates of 5200 different conformations of the FMO protein in protein data bank (PDB) format. Each of the 16 zip file contains one directory with 325 PDB files, where each file contains the coordinates of one conformation of the FMO protein. These data were generated with the FIRST/FRODA method as described in Fokas, A.S., Cole, D. and Chin, A. W. Photosynth. Res. 2014, 122, 275-292. The data were used by the present authors to explain the inhomogeneous optical properties of the FMO protein.</p>
Superb microvascular imaging (SMI) in the evaluation of musculoskeletal disorders: a systematic review
<p><strong>Objectives: </strong>To systematically review the current literature concerning the role of superb microvascular imaging (SMI), a novel Doppler technique that enables detection of fine vessels and slow blood flow, in the evaluation of musculoskeletal disorders.</p> <p><strong>Methods: </strong>An online search of the literature was conducted for the period 2013 to April 2019 and included original articles written in English language. A data analysis was performed at the end of the literature search.</p> <p><strong>Results: </strong>Eight original articles with prospective design and one with retrospective design were included in this review: 4 studies focused on rheumatoid arthritis, 2 on rheumatoid and other arthritides, 1 on lateral epicondylosis and 2 on carpal tunnel syndrome. Sample size ranged from 26 to 83 patients. Despite some methodological differences, all studies compared the performance of SMI with that of a conventional Doppler technique such as power and color Doppler and found an improvement in vascularity detection with SMI. The main variations were in sample size, evaluated parameters and vascularity interpretation methods. Inter-observer agreement for SMI ranged from moderate to excellent.</p> <p><strong>Conclusions: </strong>SMI is a promising tool for the diagnosis and treatment planning of different musculoskeletal disorders. Future investigations should include larger samples of patients with long-term follow-up.</p>
Research data for "Origins of structural and electronic transitions in disordered silicon"
<p>This is a dataset related to the publication "Origins of structural and electronic transitions in disordered silicon" (<em>Nature</em> <strong>2021</strong>, <em>589</em>, 59–64). The paper is available online here: https://doi.org/10.1038/s41586-020-03072-z.</p> <p>Three separate .tar.gz archive files are provided:</p> <ul> <li>"coordinates": structural data in (extended) XYZ format including atomic information</li> <li>"ML_DOS_data": original data for the electronic DOS analysis (Fig. 3)</li> <li>"other_potentials": tests with further ML potential models (as described in the Methods section)</li> </ul>
Decreased content of ascorbic acid (vitamin C) in the brain of knockout mouse models of Na+, K+- ATPase-related neurologic disorders
<p><strong><span><span><span><span><span><span><span><span><span><span><span>Raw data, a2Ca3-dKO phenotype and dystonic spell of a3-HT</span></span></span></span></span></span></span></span></span></span></span></strong></p> <p><strong><span><span><span><span><span><span><span><span><span><span><span>We found brain haemorrhage phenotype of Atp1a2 and Atp1a3 doule knockout (α2α3-dKO) foetuses. Here we present two kinds of α2α3-dKO line, α2-Nα3-dKO andα2-Cα3-dKO, both show brain haemorrhage upon birth. They were similar to that of homozygous knockout of the gene encoding ascorbic acid (ASC orNvitamin C) transporter, SVCT2 (SVCT2-KO). We made SVCT2-knockout mouse line by CRIPR/CAS9 method. We present SVCT2-KO, showing brain hemorrage as α2α3-dKO. The α2α3-dKO and SVCT2-KO brain showed significantly decreased level of ASC compared with the wild-type (WT) and single knockout (here, raw data). We found that the ASC content in the basal ganglia and cerebellum was significantly lower in the adult <i>Atp1a3 </i>heterozygous knockout mouse (α3-HT) than in the WT (here, raw data). We did not observe increased oxidative stress in them (here raw data). Interestingly, we observed a significant decrease in the ASC level in the basal ganglia and cerebellum of α3-HTin the peripartum period, during which mice are under physiological stress(here, raw data). Here, we show dystonic spell of α3-HT in peripartum. These observations indicate that the α2 and α3 subunits independently contribute to the ASC level in the foetal brain and that the α3 subunit contributes to ASC transport in the adult basal ganglia and cerebellum. We propose that decreases in ASC levels may affect neural network development and are linked to the pathophysiology of <i>ATP1A2- </i>and <i>ATP1A3</i>-related neurologic disorders.</span></span></span></span></span></span></span></span></span></span></span></strong></p>
Data from: Global prevalence and burden of HIV-associated neurocognitive disorder: a meta-analysis
<p>Objectives: We aimed to characterise the prevalence and burden of HAND and assess associated factors in the global population with HIV.</p> <p>Methods: We searched PubMed and Embase for cross-sectional or cohort studies reporting the prevalence of HAND or its subtypes in HIV-infected adult populations from Jan 1, 1996, to May 15, 2020, without language restrictions. Two reviewers independently undertook the study selection, data extraction, and quality assessment. We estimated pooled prevalence of HAND by a random effects model and evaluated its overall burden worldwide.</p> <p>Results: Of 5588 records identified, we included 123 studies involving 35513 participants from 32 countries. The overall prevalence of HAND was 42·6% (95% CI: 39·7-45·5), and did not differ with respect to diagnostic criteria used. The prevalence of asymptomatic neurocognitive impairment (ANI), mild neurocognitive disorder (MND) and HIV-associated dementia (HAD) were 23·5% (20·3-26·8), 13·3% (10·6-16·3) and 5·0% (3·5-6·8) according to the Frascati criteria, respectively. The prevalence of HAND was significantly associated with the level of CD4 nadir, with a prevalence of HAND higher in low CD4 nadir groups (mean/median CD4 nadir <200: 45·2%, 40·5-49·9) versus high CD4 nadir group (mean/median CD4 nadir ≥200: 37·1%, 32·7-41·7). Worldwide, we estimated that there were roughly 16145400 (95% CI 15046300-17244500) cases of HAND in HIV-infected adults, with 72% in sub-Saharan Africa (11571200 cases, 95% CI 9600000-13568000).</p> <p>Conclusions: Our findings suggest that people living with HIV have a high burden of HAND in the ART era, especially in sub-Saharan Africa and Latin America. Earlier initiation of ART and sustained adherence to maintain a high level CD4 cell count and prevent severe immunosuppression is likely to reduce the prevalence and severity of HAND.</p>
Data from: Aspirin reduces long term stroke risk in women with prior hypertensive disorders of pregnancy
OBJECTIVE: To determine if hypertensive disorders of pregnancy (HDP) increased long-term stroke risk in women in the California Teachers Study (CTS), a prospective cohort study, and if aspirin or statin use modified this risk. METHODS: CTS participants aged ≤60 years at time of enrollment in 1995 were followed prospectively for validated stroke outcomes obtained via linkage with California hospital records through 12/31/2015. We calculated unadjusted and adjusted hazard ratios (HR) and 95% confidence intervals (95%CI) for the primary outcomes of (1) all stroke and (2) stroke before age 60, among those with and without history of HDP. We tested for interactions (p<0.2) and performed stratified analyses to assess risk of the primary outcomes in women with and without self-reported use of aspirin or statins. RESULTS: Of 83,749 women included in the analysis, 4070 (4.9%) had HDP. Women with prior HDP had increased risk of all stroke (adjusted HR 1.3, 95%CI 1.2-1.4) but no increased risk of stroke before age 60 (adjusted HR 1.2, 95%CI 0.9-1.7). There was an interaction (p=0.18) between aspirin use and HDP history on risk of stroke before age 60: non-aspirin users had higher risk (adjusted HR 1.5, 95%CI 1.0-2.1) while aspirin users did not (adjusted HR 0.8, 95%CI 0.4-1.7). This effect was not seen with statins. CONCLUSIONS: Controlling for comorbidities, women with prior HDP had increased long-term stroke risk, which was reduced by aspirin use. Randomized trials may be needed to assess whether long-term aspirin use could benefit selected women with a history of HDP.
Data from: Impact of caesarean section on mode of delivery, pregnancy-induced and pregnancy-associated disorders, and complications in the subsequent pregnancy in Germany
Objectives: To analyze the impact of caesarean section (CS) on mode of delivery, pregnancy-induced and pregnancy-associated disorders, as well as complications in the subsequent pregnancy within German gynecological practices. Methods: 1,801 women with CS and 1,801 matched women with vaginal delivery (VD) from the IMS Disease Analyzer database were included. The impact of previous CS on the mode of delivery and pregnancy-associated disorders as well as complications prior to or during birth in the subsequent pregnancy were analyzed. Cox regressions were used to determine the influence of CS with regard to these outcomes. Results: Medical abortion and single spontaneous delivery were significantly less frequent in women with a history of CS compared to VD (OR equal to 0.52 and 0.04 respectively), whereas CS after CS was the significantly more common mode of delivery (79.0% versus 9.3%, OR=36.47). Gestational hypertension without significant proteinuria, gestational hypertension with significant proteinuria, and polyhydramnios were more frequent in women with CS than in women with VD (OR equal to 6.80, 1.71, and 2.29). Hemorrhage and maternal care for known or suspected disproportion were more common in the CS group than in the VD group (OR equal to 1.34 and 3.75). Prolonged pregnancy, preterm labor, abnormalities arising from forces of labor, and perineal laceration during delivery were significantly less frequent in women with CS than in women with VD (OR between 0.32 and 0.75), whereas long labor was more common (OR=2.09). Conclusion: Women with CS were more likely to undergo further CS and to develop major pregnancy-associated diseases in the following pregnancy compared to women with VD.
Data from: Disruption of the ascending arousal network in acute traumatic disorders of consciousness
Objective: To determine whether ascending arousal network (AAN) connectivity is reduced in patients presenting with traumatic coma. Methods: We performed high angular resolution diffusion imaging (HARDI) in 16 patients with acute severe traumatic brain injury who were comatose on admission and in 16 matched controls. We used probabilistic tractography to measure the connectivity probability (CP) of AAN axonal pathways linking the brainstem tegmentum to the hypothalamus, thalamus and basal forebrain. To assess the spatial specificity of CP differences between patients and controls, we also measured CP within four subcortical pathways outside the AAN. Results: Compared to controls, patients showed a reduction in AAN pathways connecting the brainstem tegmentum to a region of interest encompassing the hypothalamus, thalamus, and basal forebrain. Examining each pathway individually, brainstem-hypothalamus and brainstem-thalamus CPs, but not brainstem-forebrain CP, were significantly reduced in patients. Only one subcortical pathway outside the AAN showed reduced CP in patients. Conclusions: We provide initial evidence for the reduced integrity of axonal pathways linking the brainstem tegmentum to the hypothalamus and thalamus in patients presenting with traumatic coma. Our findings support current conceptual models of coma as being caused by subcortical AAN injury. AAN connectivity mapping provides an opportunity to advance the study of human coma and consciousness.
Data from: Increased breakdown of kynurenine towards its neurotoxic branch in bipolar disorder
Introduction Bipolar disorder (BD) is a chronic psychiatric disease which can take most different and unpredictable courses. It is accompanied by unspecific brainstructural changes and cognitive decline. The neurobiological underpinnings of these processes are still unclear. Emerging evidence suggests that tryptophan catabolites (TRYCATs), which involve all metabolites of tryptophan towards the kynurenine (KYN) branch, are involved in the etiology as well as in the course of BD. They are proposed to be mediators of immune-inflammation and neurodegeneration. In this study we measured the levels of KYN and its main catabolites consisting of the neurotoxic hydroxykynurenine (3-HK), the more neuroprotective kynurenic acid (KYNA) and anthranilic acid (AA) and evaluated the ratios between end-products and substrates as proxies for the specific enzymatic activity (3-HK/KYN, KYNA/KYN, AA/KYN) as well as 3-HK/KYNA as a proxy for neurotoxic vs. neuroprotective end-product relation in individuals with BD compared to healthy controls (HC). Methods We took peripheral TRYCAT blood levels of 143 euthymic to mild depressive BD patients and 101 HC. For statistical analyses MANCOVA's controlled for age, sex, body mass index, cardiovascular disease and smoking were performed. Results The levels of KYNA (F=5,579; p<.05) were reduced in BD compared to HC. The enzymatic activity of the kynurenine-3-monooxygenase (KMO) reflected by the 3-HK/KYN ratio was increased in BD individuals compared to HC (F=5,394; p<.05). Additionally the ratio of 3-HK/KYNA was increased in individuals with BD compared to healthy controls (F=11,357; p<.01). Discussion In conclusion our findings subserve the concept of KYN -pathway alterations in the pathophysiology of BD. We present evidence of increased breakdown towards the neurotoxic branch in KYN metabolism even in a euthymic to mild depressive state in BD. From literature we know that depression and mania are accompanied by inflammatory states which should be capable to produce an even greater imbalance due to activation of key enzymes in the neurotoxic direction of KYN -conversion. These processes could finally be involved in the development of unspecific brain structural changes and cognitive deficits which are prevalent in BD. Further research should focus on state dependent changes in TRYCATs and its relation to cognition, brain structure and staging parameters.
Adult picky eaters with symptoms of Avoidant/Restrictive Food Intake Disorder: Comparable distress and comorbidity but different eating behaviors compared to those with disordered eating symptoms
<p>Picky eaters are people who avoid many new and familiar foods because they dislike the taste, smell, texture, or appearance of many foods. When it is severe, picky eating can lead to weight loss or difficulty maintaining a healthy weight, nutritional deficiencies, dependence on supplements to get adequate nutrition or calories, or shame, anxiety, or difficulty engaging in daily life. When severe picky eating leads to these consequences, it can be diagnosed as Avoidant/Restrictive Food Intake Disorder (ARFID). People who restrict the amount of food they consume (or engage in exercise, purging, or fasting behaviors to get rid of calories after eating) because they are afraid of gaining weight or being fat are diagnosed with anorexia or bulimia when their eating leads to weight loss, nutritional problems, or interferes with life. ARFID is a new diagnosis, and in this paper, we show that 1) adults with ARFID symptoms are just as distressed, and just as likely to have symptoms of depression, anxiety, and obsessive compulsive disorder, as those with anorexia or bulimia, but that 2) adults with ARFID show very different types of eating behavior from adults with symptoms of anorexia or bulimia.</p>
ANALYSIS OF the risk factors of MUSCULOSKELETAL DISORDERS: A dataset on most challenging operations in the garments industry in Bangladesh and reported occupational discomforts by the workers.
<p>This dataset comprises the perceived most challenging operations in the garment industry and the occupational discomfort faced by the workers. Collected through participant surveys, the dataset encompasses demographic information and work related parameters.</p><p>The primary objective of this dataset is to identify and analyse the prevalence of MSDs in the most challenging operation in the garment industry. Researchers, ergonomists, and occupational health professionals can leverage this dataset to explore further for mitigating MSD risks in the industry.</p><p>This dataset can be used for finding the Ergonomic interventions and workplace improvements. It can facilitate specific interventions for solving work related diseases among the garment workers.</p><p>Anyone can use this dataset with proper citation.</p><p>Note: This dataset adheres to ethical considerations, and participant information is anonymized to ensure confidentiality.</p>
Sequence/simulation data for Direct Prediction of Intrinsically Disordered Protein Conformational Properties From Sequence
<p>This is a DOI-linked deposition of sequence/biophysical properties pairs used in the associated paper by Lotthammer et al:</p><p>Lotthammer, J. M.<strong>*</strong>, Ginell, G. M.<strong>*</strong>, Griffith, D.<strong>*</strong>, Emenecker, R. J. & Holehouse, A. S. <br>Direct Prediction of Intrinsically Disordered Protein Conformational Properties From Sequence.<br><i><strong>Nature Methods</strong></i> (<i>in press</i>), (2023).</p><p> </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.